Striking alteration of some populations of T/B cells in systemic lupus erythematosus: relationship to expression of CD62L or some chemokine receptors

Abstract

Recent studies have revealed new populations of T/B cells, including central/effector memory, follicular T cells and CXCR3+ or CXCR4+ B cells. In the present study, changes in these populations of CD4+ T cells were examined on the basis of the expression of CD62L, CCR7 and CXCR5 in patients with systemic lupus erythematosus (SLE) in relation to CCL21 and CXCL10. Changes in CXCR3+, CXCR4+ and CXCR5+ B cells were also examined. CD62L and various chemokine receptors were examined by flow cytometry analysis using monoclonal antibodies, and CCL21 and CXCL10 were examined by sandwich enzyme-linked immunosorbent assay. In patients with SLE, a decrease of naive T cells and an increase in the ratio of activated effector memory T cells were associated with an increase of CCL21 and CXCL10 in serum, although the correlation was not significant. An increase in the ratio of CXCR3+ B cells was also recognized. These results suggest that naive T cells are transferred to lymphoid tissue by CCL21, and that effector memory T cells are activated by CXCL10. It is also suggested that B cells responsive to follicular helper T cells tend to migrate to inflammatory tissue.

Defining a functionally distinct subset of human memory CD4+ T cells that are CD25POS and FOXP3NEG

“…3A and B). [38,39]. We also found that the memory/activated cells were skewed toward the CD25 NEG compartment in SLE patients compared to normal donors ( Fig.…”

“…Previous studies have shown that granzyme B is regulated in part by EOMES, while CD319 has activating properties on NKT cells, but little information regarding these two proteins is available for human CD4 + T cells [35][36][37]. [38,39]. We also found that the memory/activated cells were skewed toward the CD25 NEG compartment in SLE patients compared to normal donors ( Fig.…”

CXCR3, Inflammation, and Autoimmune Diseases

“…Henneken and colleagues noticed that contrary to RA patients, very few circulating (memory) B cells from lupus patients express high levels of CXCR3 25 . However a recent paper mentions an increase in the ratio of CXCR3 + B cells together with an increase in CXCL10 serum levels in patients with SLE 26 . These apparently contradictory results may be due to differences in flow cytometry analyses or to different clinical characteristics of the selected patients.…”

“…25 However a recent paper mentions an increase in the ratio of CXCR3 + B cells together with an increase in CXCL10 serum levels in patients with SLE. 26 These apparently contradictory results may be due to differences in flow cytometry analyses or to different clinical characteristics of the selected patients. Finally, very interesting information came out from a recent paper by Nicholas and colleagues, who showed that, in some SLE patients, a population of circulating memory B cells, expressing high levels of CD19, is enriched in autoreactivity (anti-Smith antigen B cells) and specifically expresses elevated CXCR3 levels.…”

Putative existence of reciprocal dialogue between Tfh and B cells and its impact on infectious and autoimmune disease

“…Considering the high number of Treg cells in the ATLO, we could speculate that FoxP3-expressing T cells could be precursors of Tfh cells, directly in situ, in the diseased arteries. Moreover, Tfh cells can be found in the blood of patients with SLE and Sjogren's syndrome [146,147], suggesting that, given the rising incidence of accelerated atherosclerosis in patients with SLE [131], the circulating Tfh compartment may play a role in vascular pathology too.…”