Immune response lymphoid cells

After activation, cytotoxic T cells emerge from lymphoid organs to infiltrate the graft and trigger the immune response. These cells have been shown to induce graft destruction via two mechanisms (1) secretion of the cytotoxic proteins perforin and granzyme B, and (2) induction of cellular apoptosis... 

Thus, the bulk of evidence available to date would suggest at least in mice that the spleen contains a population of thymic hormone-responsive lymphoid cells that functions mainly in the suppression of immune responses, perhaps masking concomitant helper effects. In the thymus, the predominant effects of thymic peptides appear to be the induction of functional helper cells, possibly by the enhancement of lymphokine production. The effects of thymulin, thymosin, or other thymic factors on IL-2 production may indeed represent a major function of the endocrine thymus, since IL-2 has been shown to be a potent physiological promoter of T cell maturation (Ruscetti and Gallo, 1981). 

Eisenstein TK, Hilburger ME (1998) Opioid modulation of immune responses effects on phagocyte and lymphoid cell populations. J Neuroimmunol 83 36-44 El-Hage N, Gurwell JA, Singh IN, Knapp PE, Nath A, Hauser KF (2005) Synergistic increases in intracellular Ca +, and the release of MCP-1, RANTES, and IL-6 by astrocytes treated with opiates and HIV-1 Tat. Gha 50 91-106... 

Forster R, Schubel A, Breitfeld D, et al. CCR7 coordinates the primary immune response by establishing functional microenvironments in secondary lymphoid organs. Cell 1999 99 23-33. 

Cells of the T cell lineage appear to be more sensitive to the immunomodulatory effects of Pb compared to other lymphoid populations. In addition, there are considerable differences in sensitivity across various T cell subpopulations [38 41], This differential sensitivity has become another major hallmark of Pb-induced immunotoxicity, although most data implicate T cells as indirect targets of Pb immunotoxicity. Both in vivo and in vitro observations of T-dependent immune responses in the presence of Pb suggest that T helper function and Th-dependent cytokines are skewed preferentially toward Th2 reactivities. Smith and Lawrence [42] found that Pb inhibited antigen presentation and stimulated a T cell clone of the Thl phenotype. McCabe and Lawrence [38] were the first to show that Pb inhibited Thl stimulation while it promoted presentation to Th2 clones. Heo and colleagues [39 41] provided both in vitro and in vivo results supporting this immunomodulation by Pb. 

In summary, although numerous AhR-dependent changes in the bone marrow and thymus have been found in TCDD-treated mice, it appears that these effects are self-limiting in adult mice, as T and B cell numbers are not reduced in secondary lymphoid tissue except after exposure to high doses of TCDD or in the context of an adaptive immune response. More subtle effects, such as changes in the antigenic specificity of peripheral T and B lymphocyte populations, have not been documented. 

As described previously, the humoral immune response results in the proliferation, activation, and subsequent production of antibodies by B cells following antigenic exposure and stimulation. The functionality and interplay between the three primary types of immune cells (macrophage, B cells, and T cells) required to elicit a humoral response can be assessed through various in vitro assays using cells from the peripheral blood or lymphoid tissues. 

Estrogen is one of the compounds known to modulate immune responses. Estrogenic immunosuppression was found to be due to a direct interaction with lymphoid target cells as well as via non lymphoid tissue being the thymic epithelium with its function for lymphoid maturation and selection [88]. 

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. 

---