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- Title
Das neonatale Immunsystem: Modulation durch regulatorische T-Zellen und CTLA-4 (CD152).
- Authors
Hebel, Katrin; Pierau, Mandy; Lingel, Holger; Steiner, Michael; Krause, Hardy; Jorch, Gerhard; Brunner-Weinzierl, Monika C.
- Abstract
The dysregulation of CTLA-4 (CD152), a glycoprotein expressed on the surface of lymphocytes, may lead to chronic inflammation. Based on the recent scientific findings, it has become clear that CTLA-4 inhibits the effector function and, thus, shuts down the effector phase of the T-lymphocytes. Interestingly, the CTLA-4-expressing cells become resistant to apoptosis (programmed cell death) and increasingly migrate to the lymph nodes and tissues. Studies have shown that regulatory T cells (Tregs), which switch off unwanted immune responses can inhibit in vivo only if they express an intact CTLA-4 gene. Moreover, it was confirmed that CTLA-4 is not only expressed on the T-lymphocytes but also on the B-lymphocytes. The mice with genetic inactivation of CTLA-4 in the B-lymphocytes show an increased production of the IgM antibodies after immunization. Interestingly, in particular, the B- and T-lymphocytes from the newborns and infants show a strongly increased CTLA-4 expression, suggesting a key immunoregulatory role in the neonatal immune responses. The molecules such as CTLA-4, which regulate the differentiation of the lymphocytes, could provide therapeutic targets during the early childhood to set the course for protection against autoimmunity and allergy.
- Subjects
IMMUNE system physiology; T cells; IN vitro studies; PHYSIOLOGY
- Publication
Journal of Laboratory Medicine / Laboratoriums Medizin, 2013, Vol 37, Issue 3, p123
- ISSN
0342-3026
- Publication type
Article
- DOI
10.1515/labmed-2012-0061