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Title: Differentiating the roles of STAT5B and STAT5A in human CD4(+) T cells
Authors: JENKS, Jennifer A.SEKI, ScottKANAI, TakahiroHUANG, JenniferMORGAN, Alexander A.SCALCO, Renata C.NATH, RuhiBUCAYU, RobertWIT, Jan M.AL-HERZ, WaleedRAMADAN, DinaJORGE, Alexander A.BACCHETTA, RosaHWA, VivianROSENFELD, RonNADEAU, Kari C.
Citation: CLINICAL IMMUNOLOGY, v.148, n.2, p.227-236, 2013
Abstract: STAT5A and STAT5B are highly homologous proteins whose distinctive roles in human immunity remain unclear. However, STAT5A sufficiency cannot compensate for STAT5B defects, and human STAT5B deficiency, a rare autosomal recessive primary immunodeficiency, is characterized by chronic lung disease, growth failure and autoimmunity associated with regulatory T cell (Treg) reduction. We therefore hypothesized that STAT5A and STAT5B play unique roles in CD4(+) T cells. Upon knocking down STAT5A or STAT5B in human primary T cells, we found differentially regulated expression of FOXP3 and IL-2R in STAT5B knockdown T cells and down-regulated Bcl-X only in STAT5A knockdown T cells. Functional ex vivo studies in homozygous STAT5B-deficient patients showed reduced FOXP3 expression with impaired regulatory function of STAT5B-null Treg cells, also of increased memory phenotype. These results indicate that STAT5B and STAT5A act partly as non-redundant transcription factors and that STAT5B is more critical for Treg maintenance and function in humans.
Appears in Collections:

Artigos e Materiais de Revistas Científicas - FM/MCM
Departamento de Clínica Médica - FM/MCM

Artigos e Materiais de Revistas Científicas - HC/ICHC
Instituto Central - HC/ICHC

Artigos e Materiais de Revistas Científicas - LIM/25
LIM/25 - Laboratório de Endocrinologia Celular e Molecular

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