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Immune system dysfunction and autoimmune disease in mice lacking Emk (Par-1) protein kinase
J B Hurov1, T S Stappenbeck, C M Zmasek
1Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110-1093, USA.
Abstract:
Emk is a serine/threonine protein kinase implicated in regulating polarity, cell cycle progression, and microtubule dynamics. To delineate the role of Emk in development and adult tissues, mice lacking Emk were generated by targeted gene disruption. Emk(-/-) mice displayed growth retardation and immune cell dysfunction. Although B- and T-cell development were normal, CD4(+)T cells lacking Emk exhibited a marked upregulation of the memory marker CD44/pgp-1 and produced more gamma interferon and interleukin-4 on stimulation through the T-cell receptor in vitro. In addition, B-cell responses to T-cell-dependent and -independent antigen challenge were altered in vivo. As Emk(-/-) animals aged, they developed splenomegaly, lymphadenopathy, membranoproliferative glomerulonephritis, and lymphocytic infiltrates in the lungs, parotid glands and kidneys. Taken together, these results demonstrate that the Emk protein kinase is essential for maintaining immune system homeostasis and that loss of Emk may contribute to autoimmune disease in mammals.
Insights
Mice lacking the Emk protein kinase showed immune cell dysfunction and developed autoimmune symptoms. This highlights Emk
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Emk (Emmprin kinase) is a serine/threonine protein kinase.
- It plays roles in cell polarity, cell cycle, and microtubule dynamics.
Purpose of the Study:
- To investigate the function of Emk in mammalian development and immunity.
- To understand the consequences of Emk deficiency in vivo.
Main Methods:
- Generation of Emk-deficient (Emk-/-) mice via gene targeting.
- Analysis of immune cell function, including T-cell and B-cell responses.
- Histopathological examination of aged Emk-/- mice for autoimmune manifestations.
Main Results:
- Emk-/- mice exhibited growth retardation and immune cell dysfunction.
- CD4(+) T cells showed increased memory marker (CD44/pgp-1) and cytokine production (IFN-γ, IL-4).
- Aged Emk-/- mice developed splenomegaly, lymphadenopathy, glomerulonephritis, and lymphocytic infiltrates, indicating autoimmune disease.
Conclusions:
- Emk protein kinase is crucial for maintaining immune system homeostasis.
- Loss of Emk function can lead to immune dysregulation and contribute to autoimmune conditions.
