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The top ten clues to understand the origin of chronic lymphocytic leukemia (CLL).

Abstract：

:The fundamental task of the immune system is to protect the individual from infectious organisms without serious injury to self. The essence of acquired immunity is molecular self/non self discrimination. Chronic lymphocytic leukemia is characterized by a global failure of immune system that begins with the failure of immunological tolerance mechanisms (autoimmunity) and finish with the incapacity to response to non-self antigens (immunodeficiency). Immunological tolerance mechanisms are involved in chronic lymphocytic leukemia (CLL) development. During B cell development some self-reactive B cells acquire a special BCR that recognize their own BCR. This self-autoantibody-self BCR interaction promotes survival, differentiation and proliferation of self-reactive B cells. Continuous self-autoantibody-self BCR interaction cross-linking induces an increased rate of surface BCR elimination, CD5+ expression, receptor editing and anergy. Unfortunately, some times this mechanisms increase genomic instability and promote additional genetic damage that immortalize self-reactive B cells and convert them into CLL like clones with the capability of clonal evolution and transformed CLL B cells. This review summarizes the immunological effects of continuous self-autoantibody-self BCR interaction cross-linking in the surface of self-reactive B cells and their role in CLL development.

journal_name

J Autoimmun

journal_title

Journal of autoimmunity

authors

García-Muñoz R,Feliu J,Llorente L

doi

10.1016/j.jaut.2014.10.005

subject

Has Abstract

pub_date

2015-01-01 00:00:00

pages

81-6

eissn

0896-8411

issn

1095-9157

pii

S0896-8411(14)00149-8

journal_volume

56

pub_type

杂志文章,评审

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