z-logo
Premium
Dendritic cell SIRPα regulates homeostasis of dendritic cells in lymphoid organs
Author(s) -
Washio Ken,
Kotani Takenori,
Saito Yasuyuki,
Respatika Datu,
Murata Yoji,
Kaneko Yoriaki,
Okazawa Hideki,
Ohnishi Hiroshi,
Fukunaga Atsushi,
Nishigori Chikako,
Matozaki Takashi
Publication year - 2015
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/gtc.12238
Subject(s) - cd11c , biology , microbiology and biotechnology , dendritic cell , homeostasis , immune system , cd47 , myeloid , cd8 , immunology , lymphatic system , spleen , phenotype , genetics , gene
Signal regulatory protein α ( SIRP α), an immunoglobulin superfamily protein that is expressed predominantly in myeloid lineage cells such as dendritic cells ( DC s) or macrophages, mediates cell–cell signaling. In the immune system, SIRP α is thought to be important for homeostasis of DC s, but it remains unclear whether SIRP α intrinsic to DC s is indeed indispensable for such functional role. Thus, we here generated the mice, in which SIRP α was specifically ablated in CD 11c + DC s ( Sirpa Δ DC ). Sirpa Δ DC mice manifested a marked reduction of CD 4 + CD 8α – conventional DC s ( cDC s) in the secondary lymphoid organs, as well as of Langerhans cells in the epidermis. Such reduction of cDC s in Sirpa Δ DC mice was comparable to that apparent with the mice, in which SIRP α was systemically ablated. Expression of SIRP α in DC s was well correlated with that of either endothelial cell‐selective adhesion molecule ( ESAM ) or Epstein–Barr virus‐induced molecule 2 ( EBI 2), both of which were also implicated in the regulation of DC homeostasis. Indeed, ESAM + or EBI 2 + cDC s were markedly reduced in the spleen of Sirpa Δ DC mice. Thus, our results suggest that SIRP α intrinsic to CD 11c + DC s is essential for homeostasis of cDC s in the secondary lymphoid organs and skin.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here