“The whole appeal of this Institute is that it’s small, very focused, and you have the potential for really good interactions with experts in related but diverse fields of immunology.  That’s why it does well and functions well.”  - Mick Croft, Ph.D.

Dr. Croft is a full Member in the Molecular Immunology Division of LIAI. Dr. Croft's research focus is on the cellular regulation of T cell immunity and tolerance, and how membrane bound costimulatory molecules control T cell function.

Dr. Croft received his BSc in Biology from Brunel University in London, U.K, and a Ph.D. in Immunology from Sussex University in the U.K. In 1989 he moved to the Biology Department of the University of California, San Diego as a postdoctoral fellow. In 1996, Dr. Croft joined the Immunochemistry Division of LIAI as Assistant Member, and was appointed as an Associate Member in 2001. Dr. Croft was tenured in 2003.

Dr. Croft is currently an acknowledged leader in the field of T cell costimulation and regulation of T cell immunity. He is a permanent member of one of the National Institutes of Health grant review study sections, and has served on many special emphasis panels for the NIH and for several foreign Immunology organizations. He is an Associate Editor for the Journal of Immunology.

Michael Croft, Ph.D., and his team focus on a number of protein molecules that are members of the tumor necrosis factor receptor (TNFR) family, a group of proteins believed to play important roles in the ability of the immune system to guard the body against harmful microorganisms. The TNFR molecules studied by Dr. Croft and his laboratory are expressed on T lymphocytes and may be crucial for the effective development and function of these cells.

The two molecules that are being studied most extensively are named OX40 and 4-1BB. Data from the laboratory shows that signals from both molecules control the activities and long-term survival of T cells. Specifically, both molecules may be essential for inducing immunity.

The laboratory is investigating the roles of these molecules in several diseases, including asthma, multiple sclerosis, diabetes, and cancer to determine if they could be potential targets for therapeutic intervention. Research is under way to determine whether inhibiting the activities of OX40 and 4-1BB can reduce the response of T lymphocytes.

Another line of research is investigating whether substances that can signal T cells through OX40 and 4-1BB can be used to increase natural immune responses. This is particularly important for diseases such as cancer, in which T cells do not function strongly against the growing tumor.

The role of TNF superfamily members in T-cell function and diseases. Nature Rev. Immunol. 2009

4-1BB as a therapeutic target for human disease. In Therapeutic Targets of the TNFR Superfamily. Landes Bioscience. 2009

Antagonism of airway tolerance by endotoxin/LPS through promoting OX40L and suppressing antigen-specific Foxp3+ T regulatory cells. J. Immunol. 2008

OX40 drives protective vaccinia virus-specific CD8 T cells. J. Immunol. 2008

Identification of regulatory functions for 4-1BB and 4-1BBL in myelopoiesis and the development of dendritic cells. Nature Immunol. 2008

The kinases aurora B and mTOR regulate the G1-S cell cycle progression of T lymphocytes. Nature Immunology. 2007

Signals from OX40 regulate NFATc1 and Th2 lineage commitment. PNAS. 2006

Sustained survivin expression from OX40 costimulatory signals drives T cell clonal expansion. Immunity. 2005

The costimulation-regulated duration of PKB activation controls T cell longevity.  Nature Immunology. 2004

Co-stimulatory members of the TNFR family: Keys to Effective T cell immunity. Nature Rev. Immunol. 2003

OX40 (CD134) controls memory T helper 2 cells that drive lung inflammation.  J. Exp. Med. 2003

OX40 promotes Bcl-xL and Bcl-2 expression and is essential for long-term survival of CD4 T cells. Immunity. 2001

Signaling through OX40 (CD134) breaks peripheral T cell tolerance. Nature Medicine. 2001

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