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Cited by 171

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Human CD4 helper T cell activation: functional involvement of two distinct collagen receptors, 1F7 and VLA integrin family.

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Dang, N H, Torimoto, Y, Schlossman, S F, Morimoto, C·1990·The Journal of experimental medicine

Abstract

In the present study, we showed that activation of human CD4 T cells can be induced by anti-CD3 and collagen in a serum-free system. This activation was inhibited by the addition of peptides containing the RGD or Gly-Pro-X sequences. Significantly, we demonstrated that both the 1F7 (CD26) structure and the VLA integrin family, particularly the VLA-3 complex, contribute to the functional interaction between collagen and CD4 cells since anti-1F7 and anti-VLA-3 specifically inhibited this collagen-induced CD4 cell activation. Biochemical studies showed that the 1F7 structure is not a member of the VLA integrin family. These results thus indicated that two different families of antigens serve as functional collagen receptors for CD4 T cell activation.

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Metadata

Authors
Dang, N. H., Torimoto, Y., Schlossman, S. F., & Morimoto, C.
Venue
The Journal of experimental medicine
Published
1990-08-01
Volume
172
Issue
2
Pages
649-652
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2095326273
Cited by
171
References
0
FWCI
4.20
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Human CD4 helper T cell activation: functional involvement of two distinct collagen receptors, 1F7 and VLA integrin family. https://app.cochat.ai/papers/10.1084/jem.172.2.649
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Dang, N. H., Torimoto, Y., Schlossman, S. F., & Morimoto, C. (1990). Human CD4 helper T cell activation: functional involvement of two distinct collagen receptors, 1F7 and VLA integrin family. The Journal of experimental medicine. https://doi.org/10.1084/jem.172.2.649

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.