24 research outputs found
Alterations in Mesenteric Lymph Node T Cell Phenotype and Cytokine Secretion are Associated with Changes in Thymocyte Phenotype after LP-BM5 Retrovirus Infection
In this study, mouse MLN cells and thymocytes from advanced stages of
LP-BM5 retrovirus infection were studied. A decrease in
the percentage of IL-7+
cells and an increase in the percentage of IL-16+ cells in the MLN
indicated that
secretion of these cytokines was also altered after LP-BM5 infection. The
percentage of MLN T cells expressing IL-7 receptors was significantly reduced,
while the percentage of MLN T cells expressing TNFR-p75 and of B cells
expressing TNFR-p55 increased. Simultaneous analysis of surface markers and
cytokine secretion was done in an attempt to understand whether the deregulation
of IFN-Υ secretion could be ascribed to a defined cell phenotype, concluding
that
all T cell subsets studied increased IFN-Υ secretion after retrovirus infection.
Finally,
thymocyte phenotype was further analyzed trying to correlate changes in thymocyte
phenotype with MLN cell phenotype. The results indicated that the increase in
single positive either CD4+CD8- or CD4-
CD8+ cells was due to accumulation of
both immature (CD3- ) and mature (CD3+) single
positive thymocytes. Moreover,
single positive mature thymocytes presented a phenotype similar to the phenotype
previously seen on MLN T cells. In summary, we can conclude that LP-BM5 uses
the immune system to reach the thymus where it interferes with the generation of
functionally mature T cells, favoring the development of T cells with an abnormal
phenotype. These new T cells are activated to secrete several cytokines that in turn
will favor retrovirus
replication and inhibit any attempt of the immune system to control infection
Population dynamics of CD4+ T cells lacking Thy-1 in murine retrovirus-induced immunodeficiency syndrome (MAIDS).
Increased numbers of CD4+ Thy-1- cells have been described in the spleen (SP) of mice with retrovirus-induced immunodeficiency (MAIDS). Since this phenotypic abnormality might have considerable functional importance, the expansion of the CD4+ Thy-1- subset in MAIDS was characterized further. CD4+ Thy-1- and Thy-1+ T-cells from infected mice expressed similar densities of CD3 and TCR alpha/beta. In contrast, the Thy-1- subset was uniformly CD44hi, even early in the disease when part of Thy-1+ cells were still CD44lo. The emergence of CD4+ Thy-1- cells occurred first in SP and lymph nodes and was observed later in thymus. The important fraction of CD4+ cells lacking Thy-1 normally present in Peyer's patches was only weakly modified. Despite the major expansion of the CD4+ Thy-1- phenotype, the proliferating fraction was not higher in this subset than in CD4+ Thy-1+ cells from infected mice. Persistence after hydroxyurea administration was identical in both subsets, indicating similar mean cell lifespans. Taken together, these results show that the major expansion of CD4+ Thy-1- T-cells in MAIDS is not ascribable solely to increased proliferation within this subset. Phenotypic analysis suggests that CD4+ Thy-1- cells result from the differentiation of Thy-1+ cells induced by activation signals related to retroviral infection