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B7-H1 costimulation preferentially enhances CD28-independent T-helper cell function
1Department of Immunology, Mayo Graduate and Medical Schools, Mayo Clinic, Rochester, MN 55905, USA.
Blood
|March 10, 2001
Summary
Researchers identified a mouse B7-H1 molecule that costimulates T-cell growth and cytokine secretion, revealing a unique pathway impacting T-helper cell functions independently of CD28.
Area of Science:
- Immunology
- Molecular Biology
Background:
- B7-H1 is a B7-like molecule involved in T-cell costimulation.
- Its precise role and interaction with other costimulatory molecules like CD28, CTLA-4, and ICOS are not fully elucidated.
Purpose of the Study:
- To identify and characterize the mouse homologue of human B7-H1.
- To investigate the immunologic functions of mouse B7-H1 in vitro and in vivo.
- To determine if B7-H1 mediates a unique costimulatory pathway.
Main Methods:
- Sequence analysis to identify mouse B7-H1.
- In vitro studies of T-cell proliferation and cytokine secretion.
- In vivo studies using B7-H1 transfected tumor cells and B7-H1Ig fusion protein administration.
Main Results:
- Mouse B7-H1 shares 69% amino acid homology with human B7-H1.
- Mouse B7-H1 expression on immune cells enhances T-cell proliferation and secretion of IL-10, IFN-gamma, and GM-CSF.
- B7-H1 preferentially costimulates CD4+ T cells independently of CD28 and enhances mixed lymphocyte responses.
- B7-H1 expression on tumor cells did not enhance cytolytic T-cell responses.
- B7-H1Ig fusion protein enhanced T-cell proliferation and antibody production.
Conclusions:
- A unique costimulatory pathway mediated by B7-H1 has been identified.
- This pathway preferentially affects T-helper cell functions.
- B7-H1 represents a distinct costimulatory molecule with potential therapeutic implications.