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Panminerva Medica 2001 March;43(1):1-5

Copyright © 2009 EDIZIONI MINERVA MEDICA

language: English

Th2 cytokine role in autoimmune haemolytic anaemia (AIHA) pathogenesis

Toriani-Terenzi C., Fagiolo E.

From the Laboratory of Immunohematology Catholic University of “Sacro Cuore”, Rome, Italy


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Back­ground. ­AIHA is char­ac­ter­ised by the destruc­tion of anti­body-coat­ed red ­blood ­cells, but the mech­a­nism ­that ­initiates the pro­duc­tion of auto­an­ti­bod­ies ­remains ­unclear. We ­have stud­ied the pro­life­ra­tive ­response and the spon­ta­ne­ous and mito­gen-­induced (PHA and OKT3) syn­the­sis of IFN-γ, IL-2 and IL-4 by periph­er­al ­blood mono­nu­cle­ar ­cells ­from ­patients ­with ­AIHA ­before any treat­ment to inves­ti­gate the acti­va­tion of Th1 and Th2 sub­sets.
Meth­ods. Thir­teen ­AIHA ­patients, ­both idiopath­ic and asso­ciat­ed ­with oth­er dis­eas­es, ­were stud­ied by ­ELISA meth­ods and H3 thy­mi­dine incor­po­ra­tion to deter­mine in ­vitro cyto­kine pro­duc­tion and T ­cell pro­life­ra­tive ­response, respec­tive­ly.
­Results. ­Under ­basal con­di­tions the pro­life­ra­tive ­response ­induced in periph­er­al ­blood mono­nu­cle­ar ­cells was ­enhanced in ­AIHA ­patients sug­gest­ing a ­basal ­state of hyper­ac­ti­va­tion. ­This ­increase in pro­life­ra­tive ­response can be relat­ed to the ­basal ­enhanced lev­els of IL-2 (p<0.04), a key cyto­kine, ­that reg­u­lates the ­growth, dif­fe­ren­ti­a­tion and func­tion of lym­pho­cytes. ­High IL-2 lev­els in ­AIHA ­patients super­na­tants, ­with or with­out OKT3 stim­u­la­tion, jus­ti­fy the ­high ­basal acti­va­tion of T lym­pho­cytes. ­Under ­basal con­di­tions lev­els of IFN-γ are ­decreased and IL-4 lev­els are ­increased.
Con­clu­sions. ­AIHA is char­ac­ter­ised by the destruc­tion of anti­body-coat­ed red ­blood ­cells, but the mech­a­nism ­that ­initiates the pro­duc­tion of auto­an­ti­bod­ies ­remains ­unclear. But look­ing to ­this ­data it is pos­sible to sup­pose ­that ­there is a prev­a­lent con­tri­bu­tion of Th2 lym­pho­cytes to the path­o­gen­e­sis of ­AIHA.

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