Type II membrane protein CD69 regulates the formation of resting T-helper memory

Kenta Shinoda, Koji Tokoyoda, Asami Hanazawa, Koji Hayashizaki, Sandra Zehentmeier, Hiroyuki Hosokawa, Chiaki Iwamura, Haruhiko Koseki, Damon J. Tumes, Andreas Radbruch, Toshinori Nakayama

Research output: Contribution to journalArticlepeer-review

97 Citations (Scopus)

Abstract

Memory T-helper (Th) lymphocytes are crucial for the maintenance of acquired immunity to eliminate infectious pathogens. We have previously demonstrated that most memory Th lymphocytes reside and rest on stromal niches of the bone marrow (BM). Little is known, however, regarding the molecular basis for the generation and maintenance of BM memory Th lymphocytes. Here we show that CD69-deficient effector CD4 T lymphocytes fail to relocate into and persist in the BM and therefore to differentiate into memory cells. Consequently, CD69-deficient CD4 T cells fail to facilitate the production of high-affinity antibodies and the generation of BM long-lived plasma cells in the late phase of immune responses. Thus, CD69 is critical for the generation and maintenance of professional memory Th lymphocytes, which can efficiently help humoral immunity in the late phase. The deficit of immunological memory in CD69-deficient mice also highlights the essential role of BM for the establishment of Th memory.

Original languageEnglish
Pages (from-to)7409-7414
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume109
Issue number19
DOIs
Publication statusPublished or Issued - 8 May 2012
Externally publishedYes

Keywords

  • Homing
  • Microenvironment
  • Plasmablast
  • T-B interaction
  • Trafficking

ASJC Scopus subject areas

  • General

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