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Department of Immunology, Baylor College of Medicine, Houston, TX 77030
It seems that Drs. Focosi and Petrini (1) classify T cells as helpers for B cells only when they are able to promote B cell proliferation. It is common knowledge that there are at least two different types of Th signals during T-dependent Ag-driven B cell activation and differentiation: 1) helper signals for the initial B cell activation, which mainly takes place in the T-B junction and initiates B cell proliferation; and 2) helper signals for B cell functional maturation, which mainly takes place in the germinal center (GC) and promotes B cell differentiation such as class switching and memory cell development. It has been generally accepted that GC helper T cells are critical for the survival of B cell clones that have a competitive advantage for limited Ags, leading to clonal selection and affinity maturation (2, 3, 4). Our work (5) and another publication (6) cited in the letter of Drs. Focosi and Petrini were about T helpers for the GC pathway of B cell differentiation, showing that CD4+CD57+CXCR5+ T cells are the major helpers for B cell survival and functional maturation. The work of Bouzahzah and colleagues (7) showing enhancement of B cell proliferation by CD4+CD57– T cells but not by CD4+CD57+ T cells was not contradictory to the notion that CD4+CD57+ T cells mainly provide helper signals for GC reaction. The work of Andersson and colleagues (8) studied CD57+ T cells from peripheral blood, not GC T cells as quoted by Drs. Focosi and Petrini. It should be noted that the differentiation pathways and properties of most peripheral blood CD57+ T cells are different from those of tonsil CD57+ T cells. Nevertheless, the findings of a requirement for IL-2 and supporting B cell survival by peripheral blood CD57+ T cells do not conflict with our results. Mixed results were obtained from the work of Rasheed and colleagues (9) that used total tonsil B cells instead of purified GC B cells. In addition, CXCL13 production is not exactly a good marker for Th function. The major sources of CXCL13 in the follicular area are stromal cells such as follicular dendritic cells. Therefore, the publications (7, 8, 9) referred by Drs. Focosi and Petrini as "contrary evidences" were, in fact, consistent with or complementary to our findings. In addition, there are other earlier publications that also demonstrated CD57 as a marker for GC helper T cells (10, 11, 12).
Taken together, CD4+CD45RO+CD57+CXCR5+ are currently the best available markers that define Th cells for GC response.
References
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