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Attenuation of experimental autoimmune myocarditis by blocking activated T cells through inducible costimulatory molecule pathway.

Abstract：

OBJECTIVE:Inducible costimulator (ICOS) is a member of the CD28 family. Although inflammation is an essential pathological feature of myocarditis, the role of ICOS in myocarditis remains unclear. METHODS AND RESULTS:Lewis rats were immunized on day 0 with purified porcine cardiac myosin to establish experimental autoimmune myocarditis (EAM). Flow cytometry was used to examine expression of ICOS on myocardial infiltrating cells. Anti-ICOS antibody or ICOS-immunoglobulin (ICOSIg) was administered intravenously, and rats were killed on day 14 or 21 to study effects of ICOS/ICOS-ligand (ICOSL) pathway blockade during the antigen priming phase (days 0-14) or immune response phase (days 14-21), respectively. The heart weight to body weight ratio was determined, and histological examination and echocardiogram were performed to evaluate the severity of the disease. Cytokine expression in the heart and T cell proliferation against cardiac myosin were analyzed. Flow cytometry revealed that the majority of infiltrating cells, especially CD4-positive cells, expressed ICOS. Blockade of the ICOS/ICOSL pathway during the immune response phase attenuated EAM development. However, blockade of the ICOS/ICOSL pathway during the antigen priming phase did not attenuate and exacerbate EAM. Blockade of T cell activation through ICOS suppressed expression of cytokines including INF-gamma, IL-4, IL-6, IL-10, IL-1 beta, and TNF-alpha and inhibited T cell proliferation in vitro. CONCLUSIONS:Blockade of T cell activation through ICOS during the immune response phase regulates development of EAM, and therefore, ICOS may be an effective target for treating myocarditis.

journal_name

Cardiovasc Res

journal_title

Cardiovascular research

authors

Futamatsu H,Suzuki J,Kosuge H,Yokoseki O,Kamada M,Ito H,Inobe M,Isobe M,Uede T

doi

10.1016/s0008-6363(03)00334-1

subject

Has Abstract

pub_date

2003-07-01 00:00:00

pages

95-104

issue

1

eissn

0008-6363

issn

1755-3245

pii

S0008636303003341

journal_volume

59

pub_type

杂志文章

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