CD200

From WikiMD's Wellness Encyclopedia

CD200 is a type of protein that in humans is encoded by the CD200 gene. It is also known as OX-2 membrane glycoprotein. CD200 is a member of the immunoglobulin superfamily and is involved in the regulation of immune responses.

Structure of the CD200 protein.

Structure[edit | edit source]

CD200 is a type 1 membrane glycoprotein, which contains two immunoglobulin domains. The extracellular domain of CD200 is responsible for its immunoregulatory function. It interacts with the CD200 receptor (CD200R) on the surface of certain immune cells.

Function[edit | edit source]

CD200 has been shown to play a role in the regulation of macrophage activation and function. It does this by interacting with its receptor, CD200R, which is primarily expressed on the surface of myeloid lineage cells. This interaction leads to the suppression of T cell responses and provides a mechanism for the control of inflammatory responses.

In addition to its role in controlling immune responses, CD200 has also been implicated in neuroprotection. It is expressed in various tissues including neurons, endothelial cells, and in certain tumors.

Clinical significance[edit | edit source]

Alterations in the expression of CD200 have been associated with a variety of diseases. For example, increased expression of CD200 has been observed in certain types of cancer, including melanoma, ovarian cancer, and certain types of leukemia. This overexpression may contribute to the immune evasion of these tumors.

Conversely, decreased expression of CD200 has been associated with autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. In these conditions, the lack of CD200 expression may contribute to the overactive immune response seen in these diseases.

Research[edit | edit source]

Research is ongoing to develop therapeutic strategies that target CD200 and its receptor. These strategies could potentially be used to treat a variety of conditions, from autoimmune diseases to cancer.


See also[edit | edit source]

References[edit | edit source]




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