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CBA/N mice harbour an X-linked B cell defect which is transmitted by CBA/N female mice to their hybrid male progeny. These mice mount normal responses to thymus-dependent (TD) and some thymus-independent (TI-1) antigens, while the response to TI-2 antigens is absent. Hapten-specific plaque-forming cell (PFC) responses to TD antigens can be blockaded by concomitant exposure of these mice to TI-2 antigens bearing the same hapten. This paper investigates in defective mice the blockade of their response to TNP3-LPS (trinitrophenylated lipopolysaccharide, a TI-1 antigen), imposed by DNP59-Ficoll (dinitrophenylated Ficoll, a TI-2 antigen). The effectiveness of the blocking agent, DNP59-Ficoll, differed in various inbred mouse strains: CBA/N × C3H/HeN F1 male > CBA/N female > CBA/N · C3H/HeN F1 female. The role of T cells in the observed hapten-specific blockade phenomenon was investigated using athymic CBA/N nude mice and a B cell tolerogen. Our findings indicate that T cell participation is not essential for the blockade of CBA/N PFC responses and they suggest that direct blockade of TI- and TD-responsive B cell populations is likely to occur. [ABSTRACT FROM AUTHOR]

The immunology of pregnancy has been the focus of many studies to better understand how the mother is able to tolerate the presence of a semi‐allogeneic fetus. Far from the initial view of pregnancy as a state of immunosuppression, successful fetal development from implantation to birth is now known to be under the control of an intricate balance of immune cells. The balance between pro‐inflammatory functions used to promote embryo implantation and placental development and immunosuppressive activity to maintain maternal tolerance of the fetus is an immunological phenotype unique to pregnancy, which is dependent on the time of gestation. Neutrophils are one of a host of innate immune cells detected at the maternal–fetal interface, but very little is known of their function. In this review, we explore the emerging functions of neutrophils during pregnancy and their interactions with and regulation of T cells, a key adaptive immune cell population essential for the establishment of fetal–maternal tolerance. [ABSTRACT FROM AUTHOR]

Summary: The role of antigen‐presenting cells in the skin immune system, in particular Langerhans cells and dendritic cells, has not been well defined. We recently published a study in 'Immunology' where we reported that the loss of langerin‐positive cells in the skin accelerated wound repair in the Lang‐DTR mouse. The study published here by Li, et al. reports delayed wound closure following depletion of CD11c‐positive cells in the CD11c‐DTR mouse. In this commentary, we attribute the differences between these results to several factors that differ between the studies including the depletion of different cell populations; differences in the age and the sex of mice; differences in antibiotic use between the studies; and differences in the location of the biopsies that were taken. Here, we describe the impact of these differences on wound healing and conclude that further standardization of the wound model, and further characterization of the specific cells that are depleted in these mice, is necessary to better understand how antigen‐presenting cells contribute to wound healing. [ABSTRACT FROM AUTHOR]

Summary: Advances in transcriptomics and other approaches are shedding considerable light on tissue‐resident immune cells as distinct from recirculating cells. The advances encompass antigen‐presenting cell subsets, Tregs and importantly, tissue‐resident memory cells (TRM). What are the transcriptional programmes and functional properties that distinguish the requirements for an effective tissue resident cell in brain relative to lung, skin, adipose tissue or the genital tract? Another important conundrum has been the extent to which TRM cells are specialized either as a 'sense and alarm' population or as a local, primed, effector cell population in themselves. These are questions that challenge immunologists to stop thinking in terms of a generic, model, immune response and focus instead on events in the tissue in question. [ABSTRACT FROM AUTHOR]

Summary: Severe sepsis is often accompanied by a transient immune paralysis, which is associated with enhanced susceptibility to secondary infections and poor clinical outcomes. The functional impairment of antigen‐presenting cells is considered to be a major hallmark of this septic immunosuppression, with reduced HLA‐DR expression on circulating monocytes serving as predictor of mortality. Unconventional lymphocytes like γδ T‐cells have the potential to restore immune defects in a variety of pathologies including cancer, but their use to rescue sepsis‐induced immunosuppression has not been investigated. Our own previous work showed that Vγ9/Vδ2+ γδ T‐cells are potent activators of monocytes from healthy volunteers in vitro, and in individuals with osteoporosis after first‐time administration of the anti‐bone resorption drug zoledronate in vivo. We show here that zoledronate readily induces upregulation of HLA‐DR, CD40 and CD64 on monocytes from both healthy controls and sepsis patients, which could be abrogated by neutralising the pro‐inflammatory cytokines interferon (IFN)‐γ and tumour necrosis factor (TNF)‐α in the cultures. In healthy controls, the upregulation of HLA‐DR on monocytes was proportional to the baseline percentage of Vγ9/Vδ2 T‐cells in the peripheral blood mononuclear cell population. Of note, a proportion of sepsis patients studied here did not show a demonstrable response to zoledronate, predominantly patients with microbiologically confirmed bloodstream infections, compared with sepsis patients with more localised infections marked by negative blood cultures. Taken together, our results suggest that zoledronate can, at least in some individuals, rescue immunosuppressed monocytes during acute sepsis and thus may help improve clinical outcomes during severe infection. [ABSTRACT FROM AUTHOR]

Factors influencing T-cell responses are important for vaccine development but are incompletely understood. Here, vaccinia virus (VACV) protein N1 is shown to impair the development of both effector and memory CD8+ T cells and this correlates with its inhibition of nuclear factor- κB (NF- κB) activation. Infection with VACVs that either have the N1L gene deleted (vΔN1) or contain a I6E mutation (v N1.I6E) that abrogates its inhibition of NF- κB resulted in increased central and memory CD8+ T-cell populations, increased CD8+ T-cell cytotoxicity and lower virus titres after challenge. Furthermore, CD8+ memory T-cell function was increased following infection with v N1.I6E, with more interferon- γ production and greater protection against VACV infection following passive transfer to naive mice, compared with CD8+ T cells from mice infected with wild-type virus (v N1.WT). This demonstrates the importance of NF- κB activation within infected cells for long-term CD8+ T-cell memory and vaccine efficacy. Further, it provides a rationale for deleting N1 from VACV vectors to enhance CD8+ T-cell immunogenicity, while simultaneously reducing virulence to improve vaccine safety. [ABSTRACT FROM AUTHOR]

Summary Chronic antigenic stimulation leads to gradual accumulation of late-differentiated, antigen-specific, oligoclonal T cells, particularly within the CD8+ T-cell compartment. They are characterized by critically shortened telomeres, loss of CD28 and/or gain of CD57 expression and are defined as either CD8+CD28− or CD8+CD57+ T lymphocytes. There is growing evidence that the CD8+CD28− (CD8+CD57+) T-cell population plays a significant role in various diseases or conditions, associated with chronic immune activation such as cancer, chronic intracellular infections, chronic alcoholism, some chronic pulmonary diseases, autoimmune diseases, allogeneic transplantation, as well as has a great influence on age-related changes in the immune system status. CD8+CD28− (CD8+CD57+) T-cell population is heterogeneous and composed of various functionally competing (cytotoxic and immunosuppressive) subsets thus the overall effect of CD8+CD28− (CD8+CD57+) T-cell-mediated immunity depends on the predominance of a particular subset. Many articles claim that CD8+CD28− (CD8+CD57+) T cells have lost their proliferative capacity during process of replicative senescence triggered by repeated antigenic stimulation. However recent data indicate that CD8+CD28− (CD8+CD57+) T cells can transiently up-regulate telomerase activity and proliferate under certain stimulation conditions. Similarly, conflicting data is provided regarding CD8+CD28− (CD8+CD57+) T-cell sensitivity to apoptosis, finally leading to the conclusion that this T-cell population is also heterogeneous in terms of its apoptotic potential. This review provides a comprehensive approach to the CD8+CD28− (CD8+CD57+) T-cell population: we describe in detail its origins, molecular and functional characteristics, subsets, role in various diseases or conditions, associated with persistent antigenic stimulation. [ABSTRACT FROM AUTHOR]

Human natural killer (NK) cells can be subdivided into different populations based on the relative expression of the surface markers CD16 and CD56. The two major subsets are CD56bright CD16dim/− and CD56dim CD16+, respectively. In this review, we will focus on the CD56bright NK cell subset. These cells are numerically in the minority in peripheral blood but constitute the majority of NK cells in secondary lymphoid tissues. They are abundant cytokine producers but are only weakly cytotoxic before activation. Recent data suggest that under certain conditions, they have immunoregulatory properties, and that they are probably immediate precursors of CD56dim NK cells. CD56bright NK cell percentages are expanded or reduced in a certain number of diseases, but the significance of these variations is not yet clear. [ABSTRACT FROM AUTHOR]

Cell populations of human pregnancy decidua, obtained by enzymic digestion from first trimester samples, were analysed by flow cytometry after labelling with monoclonal antibodies. The majority of these decidual cells (75%) were of bone marrow origin. The most abundant cell type expressed antigens characteristic of large granular lymphocytes (LGL), although macrophages and small numbers of classical T cells were also present. Three subsets of decidual LGL can be defined by singles and double-antibody labelling. Most decidual LGL are positive for NKH1, a marker of peripheral blood LGL, but negative for CD 16, the Fc receptor of NK cells, and for the T cell markers CD3 and CD5. About half the NKRH1-positive cells also express CD2, associated with the E-rosette receptor, and are identical to the CD3-negative/CD2-positive cells reported previously in early pregnancy decidua. The NKH1-positive cells apparently correspond to a minor subset of peripheral blood LGL. The remaining decidual LGL are positive for CD16 and negative or only dimly positive for NKH1, and are similar to the major type of peripheral blood LGL. After purification by flow cytometry, the NKH1-positive cells were demonstrated to be of similar size to, but slightly higher granularity than, lymphocytes, whereas the CD16-positive cells were larger and more granular. The possible role of decidual LGL in modulating placental development is discussed. [ABSTRACT FROM AUTHOR]

We have shown previously that staphylococcal enterotoxin S (SEB) has the capacity to non- specifically inhibit antibody responses in vitro through the induction of a suppressor cell population In the present studies, an analysis of the cellular dynamics has shown that the generation of Lyt-1-2-suppressor-effector cells is dependent on the initial activation by SEB of an Lyt- l-2- suppressor- inducer population. Co-culture experiments carried out in vitro suggest that the induction of the suppressor-effector population requires at least two signals: one signal is provided by the suppressor- inducer population, and the second signal is provided by SEW Studies also show that the in vitro antibody response is suppressed when the suppressor cells are added as late as Day 4 of a 5-day culture. While the suppressor cell population activated early in the antibody response is Lyt-1-2+, depletion studies suggest that the population that acts late in an ongoing response bears the Lyt- 1 + 2 surface phenotype. The results demonstrate that at least three distinct SEB-induced T-cell populations are capable of participating in the suppression of the antibody response. The relationship between the generation of non-specific suppressor cells and the activation of antigens specific cell circuits is discussed. [ABSTRACT FROM AUTHOR]

Mouse bone marrow cells were fractionated and enriched for functional activity as stimulators of allospecific cytolytic T-lymphocyte (CTL) responses in vitro. The relevant stimulator cells were enriched sequentially in the low-density fraction of bone marrow, its 2-hr adherent and 1 8-hr non-adherent fractions and in the FcR-negative fraction of 18-hr non-adherent cells. The functionally enriched cell population contained over 90% granulocyte precursors by ultrastructural analysis. The results indicate that granulocyte precursors are the principal cells in bone marrow that stimulate alloreactive T-cell responses. [ABSTRACT FROM AUTHOR]

Lymphoid and non-lymphoid subpopulations were investigated in the lung of the mouse with immunocyto-, immunohisto- and enzyme-histochemical methods. Special attention was paid to the cell populations in bronchus-associated lymphoid tissue (BALT), which is positioned between a bronchus and an artery. In BALT, discrete T- and B-cell areas can be found. The majority of the T cells belong to the L3T4+ (T-helper) subpopulation. In the T-cell area interdigitating cells can be recognized by anti-class II antibodies as well as by specific monoclonal antibodies, NLDC-145 and MIDC-8. Macrophage subpopulations can he discriminated by location, enzyme reactivity and various macrophage-specific monoclonal antibody markers. On the outer rim of BALT macrophages are recognized by the MOMA-1 and ERTR9 antibody. Macrophages dispersed in BALT can only be discriminated with the MOMA-2 antibody. The macrophage markers F4/80 and and Mac-1 show no reactivity in BALT. In lung, tissue macrophages around bronchi and blood vessels are predominantly recognized by the MOMA-1 and MOMA-2 antibody, and a minor population by the ERTR9 antibody. Alveolar macrophages show heterogeneity with the MOMA-1, MOMA-2 and NLDC-145 antibody. The relationship between alveolar macrophages and antigen-presenting cells is discussed here. [ABSTRACT FROM AUTHOR]

Data are presented showing that resting T cells proliferated in response to phytohaemagglutinin (PHA) provided that either sheep erythrocytes (SRC) or interleukin-2 (IL-2) was added. Proliferation requiring PHA and SRC was inhibited by anti-CD2 monoclonal antibody (OKT11) and anti-CD3 monoclonal antibody (OKT3). These monoclonal antibodies only partially inhibited IL-2 production stimulated by PHA and SRC, and added IL-2 did not restore proliferation in these cultures. Low concentrations of cyclosporine inhibited both proliferation and IL-2 production (ED50=12 and 9 ng/ml, respectively) and this inhibition was partially relieved in the presence of added IL-2 (ED50= 110 ng/ml). In contrast, proliferation stimulated by PHA with exogenous IL-2 was not inhibited in the presence of OKT11, and moderate concentrations of cyclosporine were required to inhibit proliferation (ED50= 49 ng/ml). Evidence was obtained, from analysis of cultures at limiting dilution, to suggest that the different requirements for stimulation of PHA-responsive T cells reflected different T-cell subpopulations. The majority of PHA-responsive cells proliferated in the presence of PHA and SRC, whereas only a minority proliferated in the presence of PHA and exogenous IL-2. [ABSTRACT FROM AUTHOR]

From our experiments and those of others in which cells were cultured at a density of 100,000 cells per well, it has been suggested that auto antibody production against mouse bromelain-treated erythrocytes (mouse brom-RBC) was independent of T cells, and further, was enhanced by the removal of T cells from responsive cell populations. Here it is shown in limiting dilution cultures that the autoimmune response is highly dependent on T cells or their products. B cells purified from the peritoneal cavities of untreated mice did not differentiate in vitro into autoantibody-secreting cells unless provided with signals from at least one of two types of accessory cells. These were plastic adherent cells and T cells, derived either from the peritoneal cavity or from established cell lines. Here it is shown that peritoneal T cells or T cells from the LBRM-33 cell line stimulated the differentiation of purified B cells in vitro in the absence of added mitogens. The accessory cell effect could be transferred in supernatants derived from T-cell cultures but not filler-cell cultures. Recombinant interleukin-2 (rIL-2) added to culture medium did not stimulate B cells directly, but could increase precursor frequencies when added to unfractionated peritoneal cell cultures, or B-cell cultures to which cells from a T-cell line had been added. From these results, it is concluded that the differentiation of precommitted peritoneal B cells in vitro into autoantibody secretors is at least partially dependent on T cells or lymphokines derived from them. Therefore, any proposed mechanisms for regulation of this autoimmune response should encompass the requirement for T cells or their products in the final differentiation stages to autoantibody secretion. [ABSTRACT FROM AUTHOR]

Flow cytometry was used to quantify the fluorescence of propidium iodide in rat polymorphonuclear leucocytes (PM N) attacked by the membrane attack complex (MAC) in order to establish the existence of permeability and lytic thresholds in individual cells, a `threshold' being defined as a cellular event involving the rapid transition of cells from one state to another under physiological conditions. Activation of the complement pathway resulted in PMN being attacked by MAC within 5 mm. Approximately 30-40% of the cell population subsequently became permeable to small molecules and macromolecules. Individual PMN passed through `thresholds' of cell permeability and cell lysis, or recovered from complement attack at different times. In the flow cytometer, three distinct populations of PMN were identified: (1) cells that had recovered before the permeability `threshold', (ii) cells that had recovered after the permeability `threshold' but before the lytic `threshold', and (iii) cells that failed to recover from complement attack. Individual PMN attacked by MAC passed through permeability and lytic thresholds at different times after an initial lag of 7.5 ± 2.5 mm and ll.5 ± 1.0 min, respectively. Adenosine, an activator of adenylate cyclase, inhibited removal of MAC from the cell surface. Consequently, more cells passed through the permeability and lytic `thresholds', resulting in an increased percentage of lysed cells. [ABSTRACT FROM AUTHOR]

Tumour-bearing mice produce circulating serum factors that block cell-mediated immunological reactions in vitro. The mechanism by which these specific suppressor factors (SF) block leucocyte adherence inhibition (LAI) was studied. It had previously been shown that the antigen-reactive effector cells in the LAl assay are Ly- I + T cells. We have now found that Ly-2+, I-J+ cells are required in the reactive cell population to observe the blocking action of SF from serum. Tumour-bearer spleen cells (containing Ly-2+, I-J + lymphocytes) reacted only with the specific tumour-related serum factor (SF 1) and relevant tumour antigen, to produce a non-specific suppressor factor (SF2). Specificity studies were conducted with contact-sensitized mice: hapten-specific spleen cells reacted only with hapten-related SF1 and the relevant hapten, to produce a similar SF2. SF2 differed from SF1 in suppressing allogeneic as well as syngeneic cells, in suppressing populations depleted of Ly-2+, I-J+ cells, and in being unaffected by absorption with immobilized anti-1-J antibody. Gel-filtration of SF2 revealed two forms of differing MW (> 190,000 and 20,000-50,000). [ABSTRACT FROM AUTHOR]

Small mouse lymphocytes from lymph nodes rapidly invaded three-dimensional collagen gels. In short-term assays this property was restricted to 20-25% of the cell population. Invasion was an active process involving cell locomotion. Time-lapse cinematography revealed that movement was erratic with frequent changes in cell speed. Tracks of cell paths within collagen gels demonstrated that lymphocytes made narrow angles of turn and thus showed a "persistent random-walk" similar to other cell types moving on plane substrata.

The routine bone marrow population mainly responsible for the unique competing activity of this lymphoid organ in the competition radio- immunoassay (cRIA) for AKR murine leukaemia viruses gp71 has been partially purified and characterized. That population could be distinguished by the following properties; (i) gp71+ cells (cell population expressing the AKR MuLV gp71 antigen) are mainly medium density cells, according to their distribution in the layers of a discontinuous bovine serum albumin (BSA) gradient; (ii) The gp71 positive cells are not mature lymphocytes; (iii) This cell population is found both in the FcR+ and FcR- compartments and is not included in the complement (C×) receptor-positive population; and finally, (iv) the gp71+ cells are phagocytic cells and an adherent ceil population according to its capacity to adhere to plastic surfaces, nylon wool and Sephadex G-10. [ABSTRACT FROM AUTHOR]

Thymectomized NIH and C57BL mice were more susceptible to Piasmodiurn chabaudi than controls, indicating a role for T cells in acquired immunity to the parasite. Enriched populations of T and B cells were prepared from the spleens of immune mice using nylonwool columns, and were adoptively transferred to syngeneic non-irradiated mice or mice irradiated with 600 or 800 tad. Some immunity could usually be transferred with immune T, B and glass-wool (g.w.) filtered spleen cell populations. In the heavily irradiated mice g.w. filtered immune spleen cells gave the best protection and the immune T cells the least. Preliminary attempts to show synergistic activity between immune T and B cells in irradiated mice were not successful. [ABSTRACT FROM AUTHOR]

It was found that spleen cells from mice injected i.v. with large doses of BCG respond to PHA stimulation less intensely than do normal spleen cells. We were able to show that nylon wool column purified BCG treated T cells also had a low PHA reactivity. Unfractionated spleen cells, adherent cells or T-enriched populations from BCG treated mice, when added to normal T cells lowered their PHA reactivity. When the same BCG treated cell populations were added to tumor cells in vitro, they inhibited their growth. [ABSTRACT FROM AUTHOR]

Mice infected with live Listeria monocytogenes intravenously from 1 week to 3 months following splenectomy exhibit greatly enhanced antibacterial resistance to this micro-organism as compared to normal or sham-splenectomized mice. They survive a dose of Listeria 100 times higher than is the LD50 of this parasite for normal mice. Initially, the same number of viable micro-organisms lodge in the livers of splenectomized and normal hosts. However, within 24 h after infection, the number of viable Listeria which can be recovered from the livers of splenectomized animals is significantly reduced in comparison with control mice. This effect of splenectomy is transient and gradually disappears spontaneously within 3 months following splenectomy. Enhancement of anti-listerial resistance in splenectomized mice can be abrogated by the transfer of normal spleen cells. The presence of a normal splenic cell population that controls macrophage activation is postulated. [ABSTRACT FROM AUTHOR]

The property of T cells to form rosettes with sheep red blood cells has been used to separate peripheral blood lymphocytes into purified T- and B-cell suspensions after density gradient centrifugation. A study of lymphocyte markers has shown that 2·6 per cern of E rosettes only were recovered in the B cell-enriched population. Lymphocyte stimulation in vitro was obtained with PHA. con A and PWM in unseparated and T-cell populations, but never in B-cell suspensions. Experiments of recombination between the two purified fractions have demonstrated that 10 per cent of T cells added to B cells were able to induce a response to PHA and PWM. Otherwise, only T cells responded to allogenic stimulation. Lastly, B and T cells seemed to bind qualitatively and quantitatively the same mitogens on their membranes. [ABSTRACT FROM AUTHOR]

The recovery of the B-cell population in adult thymectomized, BM mice) was studied. The irradiated and bone marrow-reconstituted mice T x number orb cells in the spleen of T × BM mice was estimated at various times after bone marrow transplantation. The spleen cells to be tested were mixed with dexamethasone-resistant thymocytes (DRT) and sheep red blood cells (SRBC) and transferred to irradiated recipients. The number of plaque-forming cells (PFC) in the spleen of the recipients was determined 7 days later. Using this functional B-cell assay a sequential appearance of the precursors of IgM-, IgGand IgA-PFC in the spleen of T × BM mice was observed. The precursors of IgM-PFC (IgM-B cells) were present immediately after transplantation. The first IgG-B cells could be detected at 13-16 days after transplantation and the IgAB cells finally appeared at 22 days after transplantation. The number of B cells reached a constant and normal level at 30 days after transplantation. The IgM-. IgG- and IgA-B cell development in sham-thymectomized, irradiated and bone marrow-reconstituted mice (ST × BM mice) was virtually the same as in T × BM mice. [ABSTRACT FROM AUTHOR]

Presents several abstracts for articles on cytokines and inflammatory responses in pregnancy. "The Maternal Inflammatory Response in Pregnancy," by G. P. Sacks, C. W. G. Redman, and I. L. Sargent; "Cytokine Production at the Maternal-Fetal Interface: Involvement of Different Cell Populations," by G. S. Vlace and P. M. Johnson; "The Endotoxin-Induced Inflammatory Response in Pregnant and Non-Pregnant Rats," by M. M. Faas; "Cytokine Transcripts in Preimplantation Embryos," by S. C. Naborska, S. E. Long, T. J. Parkinson, and M. Bailey.

The distribution and enumeration of mast cell subpopulations within the respiratory tract of a high- and low-IgE responder rat strain was determined during postnatal development. Mast cells were identified in adjacent sections by the alcian blue (AB)/safranin (SAF) staining sequence, or using immunoperoxidase to detect the rat mast cell proteinases I (RMCPI) or II (RMCPII). At birth both mucosal mast cells (MMC) and connective tissue mast cells (CTMC) were represented in very low numbers at distinct locations throughout the respiratory tract. The total number of mast cells increased with age. MMC (AB+/RMCPII+ mast cells) were the predominant phenotype in the epithelium and lamina propria of the trachea and the major conducting airways of the lung in all age groups. In contrast, CTMC (AB+/RPMCPI+ and SAF+/RMCPI+ mast cells) predominated in the submucosa of the trachea and major conducting airways as well as in the parenchyma and visceral pleura of the peripheral lung. Both phenotypes co-exist in similar proportions in peribronchial adventitial tissue and adventitia surrounding large blood vessels in neonates as well as adults. In rats the tracheal epithelium is densely populated by MMC from around the time of weaning (3 weeks) and a small but generalized increase in the number of M MC at all sites within the respiratory tract is noted from this time. This increase in MMC frequency in tissue sections with increasing age is mirrored by the levels of circulating serum RMCPII. The number of bone marrow-derived MMC also increased with increasing age prior to weaning, with a significant drop (P < 0.01) at 4 weeks of age before returning to the peak numbers in 3-week-old rats. The high-IgE responder Brown Norwegian (BN) rat strain constitutively produces significantly more IgE than the low-IgE responder White albino Glaxo (WAG) strain (P < 0.001) at all ages studied, in contrast, only minor differences between the number and distribution of mast cells in the two strains were observed. [ABSTRACT FROM AUTHOR]

A dose-dependent neutrophil migration was observed following the injection of recombinant interleukin-8 (rIL-8) into rat peritoneal cavities. This finding contrasts with the inability of rIL-8 to induce neutrophil emigration into subcutaneous air-pouches. Pre-treatment of the animals with dexamethasone (0.5 mg/kg, s.c.) or depletion of the peritoneal resident cell population abolished the neutrophil migration induced by rIL-8 and by recombinant interleukin-β (rIL-β). Different from that which occurs with rIL-β, neutrophil migration induced by rIL-8 was not enhanced by an increase in the peritoneal macrophage population. Transference of homologous total resident peritoneal cells to the air-pouch rendered this cavity responsive to the chemotactic effect of rIL-8 and potentiated the neutrophil migration induced by rIL-1. Our results show that both rIL-8 and rIL-β are able to induce in vivo neutrophil migration by an indirect mechanism, dependent on resident cells. Neither macrophages nor lymphocytes seem to be involved in the rIL-8 chemotactic effect. However, peritoneal resident mast cells may be implicated in this mechanism. These cells, when stimulated in vitro by rIL-8, released a factor that when injected into peritoneal and air-pouch cavities induced neutrophil migration. [ABSTRACT FROM AUTHOR]

Mice sensitized to oxazolone show contact sensitivity which can be assessed by painting oxazolone on the ear and measuring the increase in ear thickness at 24 hours. Contact sensitivity can be transferred passively by peritoneal exudate, lymph node and bone marrow cells. When CBA mice are challenged immediately after transfer, at a 3:1 donor recipient ratio, the peritoneal exudate cells give bigger transferred reactions than lymph node cells. The converse is true on challenge at 6 days after transfer, at which time the lymph node cells give bigger transferred reactions than the peritoneal exudate cells. These results suggest that different types or functional states of cells are involved in these two types of transfer. The possibility that the successful transfer with delayed challenge by lymph node cells was due to active sensitization by antigen transferred with the cells, was made unlikely by passive transfer into ‘tolerant’ recipients. Mice first show contact sensitivity when challenged at 3 days (about 72 hours) after sensitization. The lymph nodes develop the ability to transfer contact sensitivity with delayed challenge at the same time but the bone marrow only acquires this activity at 5 days. [ABSTRACT FROM AUTHOR]