EFFECT OF IL-7 TREATMENT ON LEISHMANIA MAJOR-INFECTED BALB.XID MICE -ENHANCED LYMPHOPOIESIS WITH SUSTAINED LACK OF B1 CELLS AND CLINICAL AGGRAVATION OF DISEASE

Citation
A. Hoerauf et al., EFFECT OF IL-7 TREATMENT ON LEISHMANIA MAJOR-INFECTED BALB.XID MICE -ENHANCED LYMPHOPOIESIS WITH SUSTAINED LACK OF B1 CELLS AND CLINICAL AGGRAVATION OF DISEASE, International immunology, 7(11), 1995, pp. 1879-1884
Citations number
38
Categorie Soggetti
Immunology
Journal title
ISSN journal
09538178
Volume
7
Issue
11
Year of publication
1995
Pages
1879 - 1884
Database
ISI
SICI code
0953-8178(1995)7:11<1879:EOITOL>2.0.ZU;2-T
Abstract
The Xid immunodeficiency was characterized by a total lack of B1 cells and reduced numbers and functions of B2 cells, In BALB,Xid mice, this defect results in an reduced susceptibility against infections with p arasites such as Trypanosoma cruzi and Leishmania major: Since IL-7 ac ts on the B cell compartment by stimulation of pre-B cell proliferatio n, we analyzed the effect of recombinant IL-7 on L. major infection in BALB.Xid mice, After application of a single dose of IL-7 simultaneou sly with the infection, the clinical course in BALB.Xid mice was marke dly aggravated, resembling that of normal BALB/c mice, IL-7-induced di sease promotion was accompanied by an up to 100-fold higher parasite l oad in several tissues of these mice, When cytokine production of puri fied, L. major-specific CD4(+) T cells from lesion-draining lymph node s was examined, the IFN-gamma production seen in untreated BALB.Xid mi ce was suppressed in IL-7-treated animals, One of the major effects of IL-7 treatment in the lymphoid organs of BALB.Xid mice was the increa se of the total number of B220, sIgM and MHC II-positive cells, These cells belonged to the B2 subset, since cells expressing surface molecu les characteristic for B1 cells (Mac-1 and Ly-1) remained absent in sp leens, lymph nodes and the peritoneum. In conclusion, selective up-reg ulation of B2 cells by IL-7 in the absence of B1 cells is associated w ith disease aggravation in L. major-infected BALB.Xid mice.