Key Role of CD36 in Toll-Like Receptor 2 Signaling in Cerebral Ischemia | Zendy

T Abe | Zendy; Munehisa Shimamura | Zendy; Katherine Jackman | Zendy; Hitomi Kurinami | Zendy; Josef Anrather | Zendy; Ping Zhou | Zendy; Costantino Iadecola | Zendy

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Key Role of CD36 in Toll-Like Receptor 2 Signaling in Cerebral Ischemia

Author(s) -

T Abe,

Munehisa Shimamura,

Katherine Jackman,

Hitomi Kurinami,

Josef Anrather,

Ping Zhou,

Costantino Iadecola

Publication year - 2010

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.109.572552

Subject(s) - tlr2 , cd36 , medicine , inflammation , ischemia , tlr4 , toll like receptor , receptor , lipopolysaccharide , innate immune system , brain ischemia , immunology , neuroscience , biology

Toll-like receptors (TLRs) and the scavenger receptor CD36 are key molecular sensors for the innate immune response to invading pathogens. However, these receptors may also recognize endogenous "danger signals" generated during brain injury, such as cerebral ischemia, and trigger a maladaptive inflammatory reaction. Indeed, CD36 and TLR2 and 4 are involved in the inflammation and related tissue damage caused by brain ischemia. Because CD36 may act as a coreceptor for TLR2 heterodimers (TLR2/1 or TLR2/6), we tested whether such interaction plays a role in ischemic brain injury.

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