Differential requirement for CD18 in T-helper effector homing.

Abstract:

:To understand the integrin requirements of T-helper (T(H)) effector subsets, we investigated the contribution of CD18 (beta(2) integrin) to T(H)1 and T(H)2 function in vitro and in relevant disease models. CD18-deficient (Itgb2(-/-)) T cells showed largely normal in vitro function. Compared with wild-type mice, Itgb2(-/-) mice were better able to resolve Leishmania major infection and generated a superior T(H)1 immune response, as assessed from draining lymph nodes. In contrast, T(H)2-dependent allergic lung disease was markedly impaired in mutant mice. In both models, development of T(H)1 and T(H)2 cells in spleens was normal, but accumulation of T(H)2 (not T(H)1) cells at inflammatory sites was reduced. Thus, CD18 is selectively required for T(H)2, but not T(H)1, homing and has a minimal influence on T-effector development. These findings suggest a new integrin-based therapeutic approach in which the outcomes of diverse diseases may be favorably influenced by altering the homing of T(H)2 cells.

journal_name

Nat Med

journal_title

Nature medicine

authors

Lee SH,Prince JE,Rais M,Kheradmand F,Shardonofsky F,Lu H,Beaudet AL,Smith CW,Soong L,Corry DB

doi

10.1038/nm932

keywords:

subject

Has Abstract

pub_date

2003-10-01 00:00:00

pages

1281-6

issue

10

eissn

1078-8956

issn

1546-170X

pii

nm932

journal_volume

9

pub_type

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