Journal
IMMUNITY
Volume 28, Issue 1, Pages 64-74Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2007.11.020
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI027811, R21AI027811] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK074738] Funding Source: NIH RePORTER
- Howard Hughes Medical Institute Funding Source: Medline
- NIAID NIH HHS [R21 AI027811, R01 AI027811, R01 AI027811-16, AI27811] Funding Source: Medline
- NIDDK NIH HHS [R01 DK074738-05, R01 DK074738] Funding Source: Medline
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Engagement of the T cell antigen receptor (TCR) during antigen presentation initiates a coordinated action of a large number of signaling proteins and ion channels. AHNAK1 is a scaffold protein, highly expressed by CD4(+) T cells, and is a critical component for calcium signaling. We showed that AHNAK1-deficient mice were highly susceptible to Leishmania major infection. AHNAK1-deficient CD4(+) T cells responded poorly to TCR stimulation in vitro with low proliferation and low Interleukin-2 production. Furthermore, AHNAK1 deficiency resulted in a reduced calcium influx upon TCR crosslinking and subsequent poor activation of the transcription factor NFAT. AHNAK1 was required for plasma membrane expression of L-type calcium channels alpha 1S (Ca(v)1.1), probably through its interaction with the beta regulatory subunit. Thus, AHNAK1 plays an essential role in T cell Ca2+ signaling through Ca(v)1 channels, triggered via TCR activation; therefore, AHNAK1 is a potential target for therapeutic intervention.
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