scholarly journals Abnormal Expression of the B-Cell Homing Chemokine Receptor BLR1 During the Progression of Acquired Immunodeficiency Syndrome

Blood ◽  
1997 ◽  
Vol 90 (2) ◽  
pp. 520-525
Author(s):  
Reinhold Förster ◽  
Georgina Schweigard ◽  
Sabine Johann ◽  
Thomas Emrich ◽  
Elisabeth Kremmer ◽  
...  
Keyword(s):  
B Cell ◽  
Chemokine Receptor ◽  
Acquired Immunodeficiency Syndrome ◽  
Peripheral Blood ◽  
Lymphoid Tissue ◽  
Healthy Individuals ◽  
T Helper ◽  
Cell Homing ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

The putative chemokine receptor BLR1 has been identified as the first G-protein–coupled receptor involved in B-cell migration and in microenvironmental homing to B-cell follicles and to germinal centers. In healthy individuals, expression of BLR1 is restricted to all mature recirculating B cells and to a subpopulation of T-helper memory cells. In the present study, we analyzed the distribution of BLR1 on defined lymphocyte subsets during the progression of acquired immunodeficiency syndrome. It is shown that the proportion of T-helper memory cells coexpressing BLR1 continuously decreases during the infection, whereas a high proportion of γ/δ T cells expressing BLR1 can be found in peripheral blood. The latter subpopulation is restricted to lymphoid tissues in healthy individuals. Most interestingly, in 75% of all human immunodeficiency virus (HIV)+ individuals, peripheral blood B cells were identified as not expressing BLR1 and phenotypically resembling germinal center cells of lymphoid tissue. Using BLR1 as a marker molecule, this study identifies peripheral blood lymphocytes in HIV+ individuals that are usually restricted to lymphoid tissue in healthy individuals. Because HIV infection is active in lymphoid tissue even at the clinically latent stage, aberrant expression of the B-cell homing chemokine receptor BLR1 might be an early indicator for the onset of destruction of lymphoid tissue.

scholarly journals Abnormal Expression of the B-Cell Homing Chemokine Receptor BLR1 During the Progression of Acquired Immunodeficiency Syndrome

Blood ◽  
1997 ◽  
Vol 90 (2) ◽  
pp. 520-525 ◽  
Author(s):  
Reinhold Förster ◽  
Georgina Schweigard ◽  
Sabine Johann ◽  
Thomas Emrich ◽  
Elisabeth Kremmer ◽  
...  
Keyword(s):  
B Cell ◽  
Chemokine Receptor ◽  
Acquired Immunodeficiency Syndrome ◽  
Peripheral Blood ◽  
Lymphoid Tissue ◽  
Healthy Individuals ◽  
T Helper ◽  
Cell Homing ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

Abstract The putative chemokine receptor BLR1 has been identified as the first G-protein–coupled receptor involved in B-cell migration and in microenvironmental homing to B-cell follicles and to germinal centers. In healthy individuals, expression of BLR1 is restricted to all mature recirculating B cells and to a subpopulation of T-helper memory cells. In the present study, we analyzed the distribution of BLR1 on defined lymphocyte subsets during the progression of acquired immunodeficiency syndrome. It is shown that the proportion of T-helper memory cells coexpressing BLR1 continuously decreases during the infection, whereas a high proportion of γ/δ T cells expressing BLR1 can be found in peripheral blood. The latter subpopulation is restricted to lymphoid tissues in healthy individuals. Most interestingly, in 75% of all human immunodeficiency virus (HIV)+ individuals, peripheral blood B cells were identified as not expressing BLR1 and phenotypically resembling germinal center cells of lymphoid tissue. Using BLR1 as a marker molecule, this study identifies peripheral blood lymphocytes in HIV+ individuals that are usually restricted to lymphoid tissue in healthy individuals. Because HIV infection is active in lymphoid tissue even at the clinically latent stage, aberrant expression of the B-cell homing chemokine receptor BLR1 might be an early indicator for the onset of destruction of lymphoid tissue.

scholarly journals Immunological abnormalities of acquired immunodeficiency syndrome and related disorders in patients from Rio de Janeiro, Brazil

1988 ◽  
Vol 83 (3) ◽  
pp. 305-311 ◽  
Author(s):  
W. Miranda-Silva ◽  
B. Galvão-Castro ◽  
M. G. Bonecini-Almeida ◽  
C. T. Daniel-Ribeiro ◽  
F. S. Sion ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Relative Increase ◽  
T Helper ◽  
Cd8 Cells ◽  
The World ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Immunological Abnormalities ◽  
Cd4 Lymphocytes ◽  
Immunological Alterations

The immunoloical profile of acquired immunodeficiency syndrome (AIDS) and chronic lymphadenopathy syndrome (CLAS) in 15 and 11 Brazilian patients, respectively, was studied. The AIDS patients showed reduced percentage of total T (CD3) and T-helper-inducer (CD4) lymphocytes, relative increase in numbers of T-suppressor-cytotoxic (CD8) cells and a marked inversion of T-helper-inducer/suppressor-cytotoxic (CD4/CD8) ratio. Lymphoproliferative responses to PHA, ConA, PPD and PWM were diminished. Hypergamaglobulinemia and high levels of circulating immune complexes were also found. The CLAS patients also showed important immunological alterations, but not so intense as those with AIDS. These data seems to be similar to those observed in other parts of the world.

Granulocyte-Macrophage Colony-Stimulating Factor Upregulates Reduced 5-Lipoxygenase Metabolism in Peripheral Blood Monocytes and Neutrophils in Acquired Immunodeficiency Syndrome

Blood ◽  
1999 ◽  
Vol 94 (11) ◽  
pp. 3897-3905 ◽  
Author(s):  
Michael J. Coffey ◽  
Susan M. Phare ◽  
Sandro Cinti ◽  
Marc Peters-Golden ◽  
Powel H. Kazanjian
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Peripheral Blood ◽  
Ex Vivo ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Acquired Immunodeficiency ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Immunodeficiency Syndrome ◽  
Stimulating Factor

Abstract Leukotrienes (LT) are mediators derived from the 5-lipoxygenase (5-LO) pathway, which play a role in host defense, and are synthesized by both monocytes (peripheral blood monocyte [PBM]) and neutrophils (PMN). Because 5-LO metabolism is reduced in alveolar macrophages and PMN from acquired immunodeficiency syndrome (AIDS) subjects, we investigated the synthesis of LT by PBM and PMN from these subjects. There was a reduction (74.2% ± 8.8% of control) in LT synthesis in PBM from human immunodeficiency virus (HIV)-infected compared with normal subjects. Expression of 5-LO (51.2% ± 8.8% of control), and 5-LO activating protein (FLAP) (48.5% ± 8.0% of control) was reduced in parallel. We hypothesized that this reduction in LT synthetic capacity in PBM and PMN was due to reduced cytokine production by CD4 T cells, such as granulocyte-macrophage colony-stimulating factor (GM-CSF). We treated 10 AIDS subjects with GM-CSF for 5 days. PBM 5-LO metabolism ex vivo was selectively increased after GM-CSF therapy and was associated with increased 5-LO and FLAP expression. PMN leukotriene B4(LTB4) synthesis was also augmented and associated with increased 5-LO, FLAP, and cytosolic phospholipase A2 expression. In conclusion, as previously demonstrated for PMN, PBM from AIDS subjects also demonstrate reduced 5-LO metabolism. GM-CSF therapy reversed this defect in both PBM and PMN. In view of the role of LT in antimicrobial function, cytokine administration in AIDS may play a role as adjunct therapy for infections.

scholarly journals In vivo treatment with interleukin 12 protects mice from immune abnormalities observed during murine acquired immunodeficiency syndrome (MAIDS).

1994 ◽  
Vol 180 (6) ◽  
pp. 2199-2208 ◽  
Author(s):  
R T Gazzinelli ◽  
N A Giese ◽  
H C Morse
Keyword(s):  
B Cell ◽  
Acquired Immunodeficiency Syndrome ◽  
Cell Activation ◽  
Interleukin 12 ◽  
B Cell Activation ◽  
Ifn Gamma ◽  
Acquired Immunodeficiency ◽  
In Vivo Treatment ◽  
Immunodeficiency Syndrome

Lymphoproliferation, chronic B cell activation resulting in hypergammaglobulinemia, and profound immunodeficiency are prominent features of a retrovirus-induced syndrome designated murine acquired immunodeficiency syndrome (MAIDS). In vivo treatment of infected mice with recombinant interleukin 12 (IL-12) beginning at the time of infection or up to 9 wk after virus inoculation markedly inhibited the development of splenomegaly and lymphadenopathy, as well as B cell activation and Ig secretion. Treatment with IL-12 also had major effects in preventing induction of several immune defects including impaired production of interferon gamma (IFN-gamma) and IL-2 and depressed proliferative responses to various stimuli. The therapeutic effects of IL-12 on the immune system of mice with MAIDS were also associated with reduced expression of the retrovirus that causes this disease (BM5def), with lesser effects on expression of ecotropic MuLV. IL-12 treatment was not effective in IFN-gamma knockout mice or in infected mice treated simultaneously with IL-12 and anti-IFN-gamma. These results demonstrate that induction and progression of MAIDS are antagonized by IL-12 through high-level expression of IFN-gamma and may provide an experimental basis for developing treatments of retrovirus-induced immune disorders with similar immunopathogenic mechanisms.

Sign in / Sign up

Export Citation Format

Share Document