Cell Mol Life Sci: Research has found that CCL21 is an attractive new target for rheumatoid arthritis treatment.

In rheumatoid arthritis (RA), the membrane tissue expresses CCL21 in large numbers, which is a coercion factor closely related to RA susceptivity.
study aims to characterifies the functional significance of CCL21/CCR7 signals at different stages of RA onset, the results of which have been published online in Cell Mol Life Sci.
study determined that CCR7 was a hallmark of RA M1 membrane fluid (SF) macrophages, and that its expression in RA monocytes and in-body differentiated macrophages was closely related to disease activity score (DAS28).
in the early days of RA, single-nucleocytes leached membrane tissue.
, blocking SF CCL21 or CCR7 prevents the migration of RA SF-mediated monocytes.
in newly migrated macrophages can be highlighted by LPS and IFN and inhibited by IL-4 therapy.
study also found that CCL21 stimulation increased the number of M1 polarized macrophages (CD14-CD86-plus), leading to higher transcriptions of IL-6 and IL-23.
these CCL21-induced M1 cytokines can differentiate childish T cells into Th17 cells without affecting the polarization of Th1 cells.
in the erosion phase of the disease, CCL21 enhances the occurrence of RA bone-breaking cells through M1-driven Th17 polarization.
by blocking IL-6, IL-23, or IL-17 functions, destroying this intricate series and impairing CCL21's ability to produce bone-breaking cells.
with in-body results, the researchers established CCL21-mediated arthritis to extend arthritis to bone erosion by connecting M1 macrophages to Th17 cell differentiation.
of the disease further exacerbated by the new angiogenesics induced by CCL21.
, the results suggest that CCL21 is an attractive new target for RA therapy because its blocking of function may eliminate aggressive arthritis regulated by M1 macrophages and Th17 cell crosstalk.
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