Polymorphism of CTLA-4 gene encoding an antigen suppressor the risk of autoimmunity

The paper presents the current state of research on the prevalence of the most commonly described polymorphism CTLA-4 gene at position 49 (G49A) in exon autoimmune diseases. Briefly discussed the mechanism of negative regulation of the immune response, in which the role of CTLA-4 (CD152). The structure CTLA-4 gene and presents the results of gene polymorphism in Addison's disease, insulin-dependent diabetes type I, Graves' disease, Hashimoto's disease, and multiple sclerosis.

The structure and biology of the T cell receptor complex (TCR/CD3)

TCR/CD3 is a complex of eight subunits that after antigen stimulation initiates a series of biochemical processes in the T cell leading to changes in cell activity . Performing the appropriate effector functions by T cells allows the specific structure in which there are two functionally distinct parts: the polymorphic region , used to recognize a specific antigen receptor ( TCR) , and a region highly conservative in signal transduction mediated T cell activation ( CD3 complex ) .

Protein p27: structure, biological functions and processes involved in the pathogenesis of proliferative

Protein p27 , belonging to the family of inhibitors of cyclin-dependent kinase called CIP / KIP , is currently the subject of intensive research in the field of cell biology and pathomechanisms of proliferative processes , because it not only controls the cell cycle by regulating the activity of CDK -cyclin complexes , but also participates in the induction apoptosis. P27 regulates the activity of CDK -cyclin holoenzymów in two ways. First, it inhibits the kinase activity of the complexes .

The Editorial Board
Andrzej Łukaszyk - przewodniczący, Zofia Bielańska-Osuchowska, Szczepan Biliński, Mieczysław Chorąży, Aleksander Koj, Włodzimierz Korochoda, Leszek Kuźnicki, Aleksandra Stojałowska, Lech Wojtczak

Editorial address:
Katedra i Zakład Histologii i Embriologii Uniwersytetu Medycznego w Poznaniu, ul. Święcickiego 6, 60-781 Poznań, tel. +48 61 8546453, fax. +48 61 8546440, email:

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