Divergent CD4+ T memory stem cell dynamics in pathogenic and nonpathogenic simian immunodeficiency virus infections

Recent studies have identified a subset of memory T cells with stem cell-like properties (T(SCM)) that include increased longevity and proliferative potential. In this study, we examined the dynamics of CD4(+) T(SCM) during pathogenic SIV infection of rhesus macaques (RM) and nonpathogenic SIV infec...

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Vydané v:The Journal of immunology (1950) Ročník 192; číslo 10; s. 4666
Hlavní autori: Cartwright, Emily K, McGary, Colleen S, Cervasi, Barbara, Micci, Luca, Lawson, Benton, Elliott, Sarah T C, Collman, Ronald G, Bosinger, Steven E, Paiardini, Mirko, Vanderford, Thomas H, Chahroudi, Ann, Silvestri, Guido
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 15.05.2014
Predmet:
Animals
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - pathology
Cercocebus atys
Immunologic Memory
Macaca mulatta
Simian Acquired Immunodeficiency Syndrome - immunology
Simian Acquired Immunodeficiency Syndrome - pathology
Simian Immunodeficiency Virus - immunology
Time Factors
ISSN:1550-6606, 1550-6606
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Shrnutí:Recent studies have identified a subset of memory T cells with stem cell-like properties (T(SCM)) that include increased longevity and proliferative potential. In this study, we examined the dynamics of CD4(+) T(SCM) during pathogenic SIV infection of rhesus macaques (RM) and nonpathogenic SIV infection of sooty mangabeys (SM). Whereas SIV-infected RM show selective numeric preservation of CD4(+) T(SCM), SIV infection induced a complex perturbation of these cells defined by depletion of CD4(+)CCR5(+) T(SCM), increased rates of CD4(+) T(SCM) proliferation, and high levels of direct virus infection. The increased rates of CD4(+) T(SCM) proliferation in SIV-infected RM correlated inversely with the levels of central memory CD4(+) T cells. In contrast, nonpathogenic SIV infection of SM evidenced preservation of both CD4(+) T(SCM) and CD4(+) central memory T cells, with normal levels of CD4(+) T(SCM) proliferation, and lack of selective depletion of CD4(+)CCR5(+) T(SCM). Importantly, SIV DNA was below the detectable limit in CD4(+) T(SCM) from 8 of 10 SIV-infected SM. We propose that increased proliferation and infection of CD4(+) T(SCM) may contribute to the pathogenesis of SIV infection in RM.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
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content type line 23
ISSN:1550-6606
1550-6606
DOI:10.4049/jimmunol.1303193