PubMed · 16109359
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Michael P Pender. 2005. CSF testing for multiple sclerosis.. https://doi.org/10.1016/s1474-4422(05)70151-4
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BACKGROUND: Several reports suggest that the dissemination of neoplastic cells and cancer progression are associated with the generation of an immunosuppressive environment. METHODS: In this report, we investigated immunological effects of prostate cancer by comparing metastastic and non-metastatic pelvic lymph nodes (LNs) from 25 patients with carcinomatous involvement of LNs to the non-metastatic LNs from 26 control patients with no metastatic involvement by immunohistochemistry and histological analyses. RESULTS: Our results showed a decreased abundance of CD20+ B lymphocytes (P = 0.031), CD38+ activated lymphocytes (P = 0.038), and CD68+ macrophages (P < 0.001), and less evidence of follicular hyperplasia (P = 0.014), sinus hyperplasia (P < 0.001), and fibrosis (P=0.028) in metastatic LNs comparatively to control LNs. Finally, we observed that metastatic LNs were significantly smaller than control LNs (P = 0.005). CONCLUSIONS: Our results suggest that the development of prostate cancer LN metastasis is accompanied with smaller LN size and decreased LN reactivity suggesting the development of an immununosuppressive microenvironment.
Idiopathic CD4+ T lymphocytopenia (ICL) is a rare heterogeneous disorder defined by CD4+ T-cell counts below 300 cells/muL in the absence of human immunodeficiency virus (HIV) infection or other known immune deficiency disorders. Here, we report the expansion of immature/transitional B cells in patients with ICL, which is associated with elevated serum levels of IL-7. Both the percentage of immature/transitional B cells and levels of IL-7 were inversely correlated with levels of CD4+ T-cell counts and directly correlated to each other. Further analyses of B cells indicated that, in contrast to the activating effects of HIV disease on mature B cells, the expansion of immature/transitional B cells in patients with ICL occurred at the expense of memory B cells. These findings extend previous reports on primary immunodeficiencies as well as HIV disease by suggesting that CD4+ T-cell lymphopenia has an impact on human B-cell development either directly or indirectly via the associated elevation of IL-7 levels.
IL-21 is a cytokine produced by CD4+ T cells that has been reported to regulate human, as well as, mouse T and NK cell function and to inhibit Ag-induced IgE production by mouse B cells. In the present study, we show that human rIL-21 strongly enhances IgE production by both CD19+ CD27- naive, and CD19+ CD27+ memory B cells, stimulated with anti-CD40 mAb and rIL-4 and that it promotes the proliferative responses of these cells. However, rIL-21 does not significantly affect anti-CD40 mAb and rIL-4-induced Cepsilon promoter activation in a gene reporter assay, nor germline Cepsilon mRNA expression in purified human spleen or peripheral blood B cells. In contrast, rIL-21 inhibits rIL-4-induced IgE production in cultures of PBMC or total splenocytes by an IFN-gamma-dependent mechanism. The presence of a polymorphism (T-83C), in donors heterozygous for this mutation was found to be associated not only with lower rIL-21-induced IFN-gamma production levels, but also with a lower sensitivity to the inhibitory effects of IL-21 on the production of IgE, compared with those in donors expressing the wild-type IL-21R. Taken together, these results show that IL-21 differentially regulates IL-4-induced human IgE production, via its growth- and differentiation-promoting capacities on isotype-, including IgE-, committed B cells, as well as via its ability to induce IFN-gamma production, most likely by T and NK cells, whereas the outcome of these IL-21-mediated effects is dependent on the presence of a polymorphism in the IL-21R.