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Increased inherent intestinal granzyme B expression may be associated with SIV pathogenesis in Asian non‐human primates
Author(s) -
Hutchison A.T.,
Schmitz J.E.,
Miller C.J.,
Sastry K.J.,
Nehete P.N.,
Major A.M.,
Ansari A.A.,
Tatevian N.,
Lewis D.E.
Publication year - 2011
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1111/j.1600-0684.2011.00482.x
Subject(s) - lamina propria , granzyme b , biology , granzyme , pathogenesis , simian immunodeficiency virus , immunology , intestinal mucosa , granzyme a , virology , immune system , cd8 , medicine , epithelium , genetics , perforin
Background Unlike Asian non‐human primates, chronically SIV‐infected African non‐human primates (NHP) display a non‐pathogenic disease course. The different outcomes may be related to the development of an SIV‐mediated breach of the intestinal mucosa in the Asian species that is absent in the African animals. Methods To examine possible mechanisms that could lead to the gut breach, we determined whether the colonic lamina propria (LP) of SIV‐naïve Asian monkeys contained more granzyme B (GrB) producing CD4 T cells than did that of the African species. GrB is a serine protease that may disrupt mucosal integrity by damaging tight junction proteins. Results We found that the colonic LP of Asian NHP contain more CD4 + /GrB + cells than African NHP. We also observed reduced CD4 expression on LP T cells in African green monkeys. Conclusion Both phenotypic differences could protect against SIV‐mediated damage to the intestinal mucosa and could lead to future therapies in HIV + humans.