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Our earlier observations indicate that adoptive transfer of spleen cells obtained from dengue type 2 virus (DV)-primed mice suppressed DV antigen-specific antibody secretion as detected by Jerne PFC technique. Findings of this paper indicate that the suppression was produced by non-glass-adherent cells, macrophage-depleted (by carbonyl iron) cells and by T lymphocytes of the spleen but not by the glass-adherent cells and B lymphocytes. The activity of these cells is dependent upon production of prostaglandin as shown by abrogation of their suppressor activity by pre-treatment of cells by indomethacin or aspirin which are known to block synthesis of prostaglandins. [ABSTRACT FROM AUTHOR]

This paper investigates desensitization in vitro, e.g. the inhibition of the transfer of contact sensitivity to picryl chloride by incubation of the passive transfer population with picrylated spleen cells. It asks whether desensitization is based on the same T-suppressor circuit which is responsible for the inhibition of passive transfer by antigen-specific T-suppressor factor (TsF). In this circuit, the T-suppressor cell which acts at the efferent stage (Ts-eff) makes TsF. This TsF depresses contact sensitivity indirectly by arming a T-acceptor cell (Tacc). The armed Tacc, when exposed to antigen (picrylated spleen cells), liberates a non-specific inhibitor which blocks the transfer of contact sensitivity. The three elements of this T-suppressor circuit occur in nylon wool-purified T cells prepared from the lymph nodes and spleens of mice four days after immunization with picryl chloride. This population transfers contact sensitivity and can be desensitized in vitro. It contains Ts-eff which can be isolated by panning (adherence) on picrylated albumin and detected by their ability to inhibit passive transfer. The 24 hr supernatant of cultures of these cells contains TsF. Finally the population contains Tacc which appear in the spleen 2 days after immunization and virtually disappear by 10 days. Further experiments demonstrated that the Ts-eff and the Tacc were not merely present but actually required for desensitization in vitro. Immune cells depleted of both Ts-eff (by panning on picrylated albumin) and Tacc (by arming with anti-oxazolone TsF and panning on oxazolonated albumin) cannot be desensitized. To restore desensitization both Ts-eff and Tacc must be added back. The Ts-eff were characterized as cyclophosphamide resistant, adult thymectomy sensitive cells (Cyr, ATx5), which adhered to antigen and were produced only by specific immunization. The Tacc were characterized as CF5, ATx5 cells which adhered to antigen only after arming with antigen-specific T-suppressor factor and were produced after immunization with an unrelated contact sensitizer, 'oxazolone'. It was concluded that desensitization in vitro was due to the interaction of two distinct T cells: the T-suppressor cell which acts at the efferent stage of the contact sensitivity reaction and the T-acceptor cell which becomes armed with the specific T-suppressor factor produced by the Ts-eff. [ABSTRACT FROM AUTHOR]

Fufang Shatai Heji (STHJ) is a mixture of traditional Chinese medicines, such as Radix Adenophorae, Radix Pseudostellariae, and Radix Astragali. STHJ is commonly used to treat diseases caused by low immune function, for example, Sjögren's syndrome (SS). The primary objective of this study was to assess the immunopotentiating effect of STHJ using an immunosuppressive mouse model receiving cyclophosphamide (CTX). Following CTX treatment, STHJ was administered by oral gavage for 30 consecutive days. The percentage of specific lymphocyte subpopulations in the spleen was measured by flow cytometry. Levels of inflammatory factors in serum were detected by enzyme-linked immunosorbent assays (ELISAs). The administration of STHJ significantly elevated thymus and spleen indices, increased B cell and natural killer (NK) cell activities, and decreased CD8+ T, CD8+CD122+ T, NKT, and γδT cell activities in the CTX-treated mice. In addition, STHJ upregulated the expression of interleukin- (IL-) 2, IL-6, and tumor necrosis factor-α (TNF-α) and downregulated IL-10 expression in CTX-treated mice. In conclusion, STHJ effectively remitted CTX-induced immunosuppression by modulating the balance of lymphocyte subsets and cytokines. Our results suggest STHJ treatment could be used as an effective therapeutic approach to improve immune function in patients with low immunity. [ABSTRACT FROM AUTHOR]

Alveolar macrophages (AM) from normal rats suppressed antigen- or mitogen-stimulated blastogenie responses in cultures of splenic or lymph node lymphocytes, high levels of suppression often being observed when added AM comprised as few 0·6% of the total cells in culture. The efficiency of AM- mediated suppression of spleen cell blastogenesis declined with the age of the spleen cell donors, was severely curtailed by pretreatment of donors with low levels of cyclophosphamide, and was depleted by adult thymectomy coupled with thoracic duct drainage. The suppressive activity of AM was most obvious at high cell density, was unaffected by the presence of indomethacin in the cultures, or by prior X-irradiation of the spleen cells. Fractionation of spleen cells by velo- city sedimentation yielded cell populations of greatly varying sensitivities to AM-mediated suppression. from small splenocytes (sedimentation velocity 1·1 - 2.8 mm/h) which were almost totally refractory to AM-suppression when assayed in isolation from the remainder of the spleen cell population, to larger cells (sedimentation velocity>3·5 mm/h) exhibiting high levels of sensitivity. Fractionation of spleen cells by glass wool adherence indicated decreased sensitivity to AM-suppression in the effluent population. Examina- tion of the suppressive activity of individual subpopulations of AM separated by velocity sedimentation indicated that the larger macrophages were the most active in vitro. Suppressive activity of this nature was not seen with unstimulated peritoneal macrophages, hut was observed when ‘activated’ peritoneal exudate cells were tested. These data are discussed in terms of a two-cell model for suppression of blastogenesis, the ultimate effector cell being a macrophage, the activity of which is controlled by a long-lived, recirculating lymphocyte, which we have provisionally designated as a T lymphocyte. [ABSTRACT FROM AUTHOR]

Antigen-dependent localization of 51Cr- labelled lymphocytes, and the subsequent uptake of IUdR into lymphoid organs has been studied as a function of age. Measures of cell localization indicated that while old age can alter the patterns of entry of lymphocytes into lymph nodes and spleen. these changes are variable and probably not sufficient alone to explain decreased primary antibody responses in old animals. Proliferation of cells, however, was cone sistently affected in both organs and this phenomenon is discussed in terms of abnormal T-cell function. [ABSTRACT FROM AUTHOR]

Antisera were prepared against a variety of chicken tissues with a view to detecting antigens specific for subpolpulations of T and B cells at different maturation stages. By appropriate absorption analysis, the following antigens were defined: (a) thymus organ-specific antigen (CTOA); (b) T lymphocyte-specific antigen (CTLA); (c) B lymphocyte-specific antigen (CBLA); (d) mature B lymphocyte-specific antigen (CBLA); (e) a foetal-associated antigen (CFAA) present on embryonic haemopoietic cells, and adult bone marrow and immature bursa cells, suggesting the cell types concerned may be at an early stage of development, possibly including precursors. For comparison with the above antigens, cells were also examined for surface Ig and IgG. T cells were found in periarteriolar sheaths in the spleen, and predominantly in the sub-epithelium and sub-mucosa of the caecal tonsil of the gut-associated lymphoid tissue (GALT). B cells were localized in periellipsoidal sheaths and germinal centers in the spleen, and in primary follicles or germinal centers in the GALT. The thymic and bursal medullas contained the mature populations of T and B lymphocytes respectively. [ABSTRACT FROM AUTHOR]

Male and female spleen cells were compared before and after culture for their cytotoxicity to autologous-embryo fibroblasts. Cultures of male cells developed significantly greater reactivity than cultures of female cells. Moreover, while the cytotoxicity derived from cultures of male cells was totally abolished by treatment of effector cells with a mouse anti-T cells antiserum, such an antiserum had less affect on the effector cells of female mouse cultures. [ABSTRACT FROM AUTHOR]

The cross reactivity of sera from rabbits sensitized to performic acid oxidized ferredoxin (O-Fd) and of spleen cells from mice sensitized to O-Fd was analysed using several chemically modified forms of ferredoxin in the complement fixation test and the in vitro lymphocyte stimulation assay. Only O-Fd and native ferredoxin (native-Fd) gave positive responses in both assays. Dinitrophenylated-O-Fd (DNP-O-Fd) and acid precipitated ferredoxin (TCA-Fd) were able to fix complement (C') but did not simulate DNA synthesis in vitro. Ferredoxin alkylated with N-ethylmaleimide (NEM-Fd) induced cell transformation but fixed C' poorly. Carboxymethylated ferredoxin (CM-Fd) was unable to stimulate DNA synthesis and was marginally able to fix C'. Methylated-O-Fd (meth-O-Fd) was not recognized in either assay. The various ferredoxin preparations were tested for their ability to sensitize mice for use in the in vitro lymphocyte stimulation assay. Only O-Fd, NEM-Fd and native-Fd were capable of sensitizing lymphocytes for a proliferative response in vitro to the test antigens. This correlates with the observation that only these antigens were able to induce DNA synthesis in O-Fd-sensitized lymphocytes. The nature of the cells responding in vitro was examined by treating the cells with rabbit antimouse irranunoglobulin and C' or rabbit anti-mouse brain associated θ and C'. The 24-hr response was found to be sensitive to both sera while the 120-hr response was sensitive only to the anti-θ sera. [ABSTRACT FROM AUTHOR]