Presence of Circulating CD4+CD28 Null T Helper Lymphocytes in Patients With Autoimmune Hemolytic Anemia.

Autoimmune hemolytic anemia (AIHA) has always been considered the simplest and most scholastic example of antibody-mediated autoimmune disease.It has been identified as a greatly heterogeneous disease, due to several immunological mechanisms involved beyond antibodies, complement and antibody-dependent cell-mediated cytotoxicity (ADCC). AIHAs may be Idiopathic of unknown cause Secondary associated with several conditions : (lymphoproliferative, autoimmune , infectious diseases, immunodeficiencies, solid tumors, transplants, and drugs).Several subsets of T and B lymphocytes with highly specialized functions have been characterized. Some lymphocytes promote inflammation, while others have anti-inflammatory roles, and an optimal balance between these two opposing sets of lymphocytes is critical for immune homeostasis. A pro-inflammatory subset of CD4+ T helper 1 (Th1) lymphocytes known as cluster of differentiation 4 positive 28 negative T helper lymphocytes (CD4+CD28 null T cells) because they characteristically lack CD28 which is a co-stimulatory receptor critical for the activation and function of T cells.CD4+CD28 null T cells are rare in healthy individuals, but they increase in inflammatory and immune-mediated diseases. Prevalence of CD4+CD28 null T cells is high in chronic inflammatory diseases, autoimmune diseases, immunodeficiency and specific infectious diseases.It remains controversial whether CD4+CD28null T cells are antigen specific and which are the precise antigens that trigger their expansion. It has been suggested that CD4+CD28null T lymphocytes are auto-reactive and that repeated stimulation by auto-antigens drives the expansion of this cell subset.Expansion of the CD4+CD28 null T-cell subset in patients affected by autoimmune disorders has been linked to the severity of disease and an unfavourable prognosis.