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This immunization team-based learning (TBL) resource allows students to use their knowledge of the principles of vaccine construction and immunization as it applies to the prevention of infectious disease. It also familiarizes the students with immunization schedules provided by the Centers for Disease Control. The unit consists of a prereading assignment where students use a detailed set of objectives to guide their reading and prepare for subsequent group activities, a readiness assurance test that assesses the student's proficiency of the prereading material, and a group application exercise that applies vaccination choices and the reasoning behind immunization schedules in five clinical scenarios. Most medical students are familiar with vaccines and immunization, if only from personal experience. This TBL expands on that experience by focusing on the underlying basic science principles used in the design, selection, and delivery of vaccines and immunization choices for different individuals.

In a murine model of autoimmunity targeted against the epidermal cell Ags, Skn, adoptive transfer of Skn-immune T cells to immunosuppressed recipients elicits skin lesions in areas of mild epidermal trauma. In this study, we examined peripheral regulation of Skn-induced autoreactivity disrupted by rendering the mice immunoincompetent. We found that regulation of Skn-directed autoimmunity was restored by cotransfer of normal syngeneic spleen cells at twice the concentration of Skn-immune cells and was evidenced by significantly reduced lesion severity by days 5–7 post-cotransfer compared with animals given injections of Skn-immune cells alone. Enrichment and depletion of normal CD4+ or CD8+ spleen cells and RT-PCR analysis of selected cytokines identified CD4+ cells as the regulatory cells in the cotransfer inoculum; however, significant reduction in lesion severity was observed only when there was a concomitant increase in levels of IL-7. The role of IL-7 was further supported in that mice cotransferred with Skn-immune cells plus normal spleen cells, but also treated with anti-IL-7 Ab, no longer exhibited reduced lesion severity. To determine whether IL-7 expression without normal spleen cell cotransfer could modulate lesion development, an IL-7-encoding plasmid (pCMV-Tag1-IL-7) was topically delivered to sites flanking the stressed skin site in Skn-induced autoimmune mice. Daily application of 15 μg of pCMV-Tag1-IL-7 significantly suppressed lesion severity. Our results support a mechanism for CD4+ T cells and IL-7 in contributing to the control of autoreactivity.

While pathogenic T cells have been identified for several diseases with epithelial cell damage, an autoimmune T cell-mediated response targeted against a known keratinocyte antigen has not been reported. Previously we described an autoimmune response directed to the mouse epidermal cell antigens, Skn. For our murine model, primed Skn-immune lymphocytes are adoptively transferred to recipients, which develop lesions at the site of mild skin trauma. In this study we investigated the nature of the autoimmune component of the Skn response. A time-course study demonstrated a relationship between the number of primed Skn-immune cells injected and the severity of skin lesions in the recipients. Immunohistochemical staining revealed the presence of both CD4+ and CD8+ T cells in lesional skin, with a predominance of CD4+ T cells. To support a role for CD4+ T cells in the initiation of the autoimmune response, Skn-immune donor cells were either enriched or depleted of various subsets prior to transfer into recipients, which showed that CD4+, but not CD8+, T cells were essential for induction of lesions. Analysis of mRNA for T-helper (Th) cell cytokines in lesional skin displayed a Th 1 bias, and treatment with cyclosporin A (CsA) or anti-interleukin (IL)-2 antibody controlled the development of lesions. Overall the results clearly show an immunopathogenic profile consistent with a T cell-mediated mechanism.

Helicobacter pylori infection has been implicated in the development of gastrointestinal malignancy in adults and children. The histopathological processes that lead to such development are unknown. We compared the immune cell repertoire of mucosal lymph follicles in children with H. pylori infection to B cell type mucosal associated lymphoid tissue (MALT)-lymphoma of adults. The B and T cell populations residing within the lymph follicles and/or within B cell type MALT lymphoma were characteriZed by an immunohistochemical technique, utilizing B and T cell markers including: CD3, CD4, CD8 (T cells); CD20, CD40, GD74, BLA36, CD80, CD86 (B cells). Stain intensity was compared between the samples. T cell repertoire was observed within the lymph follicles, but not in the B cell MALT-lymphoma specimens. No significant difference was observed between the staining of CD40, CD74, CD8, and BLA36. The B cell markers, CD80 and CD86, were found within the centrocytic zone of the lymph follicle. In the B cell repertoire, no significant difference was observed between the lymph follicles of children with H. pylori infection and the adult MALT-lymphoma specimens except in CD20. B and T cells were in close anatomical proximity, enabling them to interact and exchange immunological information.

Objectives:Candida albicansis known to produce gliotoxin, which has several prominent biological effects, including immunosuppression. interference with host defenses may arise from the effects of this toxin on leukocyte structure and function.Methods:Flow cytometric analysis revealed that polymorphonuclear leukocytes (PMN) were more sensitive to gliotoxin than were mononuclear cells. Structural and various functional aspects of PMN exposed to gliotoxin were studied.Results:Gliotoxin at (1 μg/mL) did not affect the viability but did diminish PMN chemotaxis and reduced their ability to ingest particles. Other functional aberrations included decreased nitroblue tetrazolium dye reduction, decreased superoxide production, and release of lactoferrin suggesting by degranulation. Gliotoxin also affected the ability of PMN to killEscherichia coli.Conclusions:This study suggests a previously unrecognized potential virulence factor ofC. albicansthat could contribute to persistence of yeast colonization or recurrence of symptomatic infection through diminished host resistance.

T and B Cells Repertoire in Gastric Lymph Follicles in Children with Helicobacter Pylori Infection

Rejection of murine skin grafts by hematopoietic chimeras that are fully compatible genetically with the skin-graft donor has been attributed to a disparity in skin-selective alloantigens between the irradiated host and the skin graft donor, Monoclonal antibodies recognizing Skna alloantigen were produced and used in indirect immunofluorescent and immunoperoxidase tests with sections of skin to demonstrate and confirm the expression of Skna alloantigen on epidermal cells of Skna genotype and absence of Skna alloantigen from epidermal cells of non-Skna genotype.

C57BL/6 (B6) mice that were lethally irradiated and reconstituted with (B6XA/J)F1 spleen cells were immunized against the skin-specific antigens, Skn, by grafting with A/J tail skin. Serum from these mice was shown to contain Skna-specific antibody by a flow cytometric assay using indirect immunofluorescence.