HIV Type 1-Induced Inhibition of CD45 Tyrosine Phosphatase Activity Correlates with Disease Progression and Apoptosis, but Not with Anti-CD3-Induced T Cell Proliferation

2000 ◽  
Vol 16 (3) ◽  
pp. 211-219 ◽  
Author(s):  
Antonello Giovannetti ◽  
Marina Pierdominici ◽  
Francesca Mazzetta ◽  
Anna Maria Mazzone ◽  
Giovanni Ricci ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Disease Progression ◽  
Phosphatase Activity ◽  
Tyrosine Phosphatase ◽  
T Cell Proliferation ◽  
Hiv Type 1

scholarly journals T-cell mediated autoimmunity to the insulinoma-associated protein 2 islet tyrosine phosphatase in type 1 diabetes mellitus

1999 ◽  
pp. 272-278 ◽  
Author(s):  
F Dotta ◽  
S Dionisi ◽  
V Viglietta ◽  
C Tiberti ◽  
MC Matteoli ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Type 1 Diabetes ◽  
T Cell ◽  
T Lymphocyte ◽  
Tyrosine Phosphatase ◽  
T Cell Response ◽  
T Cell Proliferation ◽  
Diabetic Patients ◽  
Hla Dr

The target molecules of the T-cell response in type 1 diabetes, despite their pathogenic importance, remain largely uncharacterized, especially in humans. Interestingly, molecules such as insulin and glutamic acid decarboxylase (GAD) have been shown to be a target not only of autoantibodies, but also of autoreactive T-lymphocytes both in man and in the non-obese diabetic (NOD) mouse. In the present study we aimed to determine the existence of a specific T-cell response towards the insulinoma-associated protein 2 (IA-2) islet tyrosine phosphatase, a recently identified autoantigen which is the target of autoantibodies strongly associated with diabetes development. Human recombinant IA-2 produced in Escherichia coli, was tested for its reactivity with peripheral blood lymphocytes obtained from 16 newly diagnosed type 1 diabetic patients and from 25 normal controls, 15 of whom were HLA-DR-matched. A T-cell proliferation assay was performed in triplicate employing freshly isolated cells in the absence or in the presence of the antigen to be tested (at two different concentrations: 2 microg/ml and 10 microg/ml). A specific T-cell proliferation (defined as a stimulation index (S.I.) >/=3) was observed against IA-2 used at a concentration of 10 microg/ml (but not of 2 microg/ml) in 8/16 diabetic patients, in 1/15 HLA-DR-matched control subjects (P<0.01 by Fisher exact test) and in 0/10 of the remaining normal individuals. A statistically significant difference (P<0.003 by Mann-Whitney U test) was also observed in S.I. values between patients (3.1+/-1.4) and HLA-DR-matched controls (1.7+/-0.54) employing IA-2 at a concentration of 10 microg/ml. However, when IA-2 was used at a concentration of 2 microg/ml, the difference in S. I. between patients (1.65+/-0.8) and controls (1.0+/-0.3) did not reach statistical significance. In conclusion, these data show the presence of a specific, dose-dependent T-lymphocyte response against the IA-2 islet tyrosine phosphatase at the onset of type 1 diabetes. Consequently, this molecule appears to be a target not only at the B-lymphocyte but also at the T-lymphocyte level, reinforcing the potential pathogenic role of this autoantigen in the islet destructive process.

scholarly journals Regulatory T Cell Expansion and Immune Activation during Untreated HIV Type 1 Infection Are Associated with Disease Progression

2009 ◽  
Vol 25 (2) ◽  
pp. 183-191 ◽  
Author(s):  
Weiwei Cao ◽  
Beth D. Jamieson ◽  
Lance E. Hultin ◽  
Patricia M. Hultin ◽  
Roger Detels
Keyword(s):  
T Cell ◽  
Disease Progression ◽  
Immune Activation ◽  
Regulatory T Cell ◽  
Cell Expansion ◽  
Hiv Type 1 ◽  
T Cell Expansion

scholarly journals Homeostatic T Cell Proliferation after Islet Transplantation

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Paolo Monti ◽  
Lorenzo Piemonti
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Islet Transplantation ◽  
T Cell Proliferation ◽  
Pancreatic Islet Transplantation ◽  
Therapeutic Approaches ◽  
Cell Responses ◽  
New Therapeutic Approaches ◽  
Alloreactive T Cell

Pancreatic islet transplantation in patients with type 1 diabetes mellitus is performed under immunosuppression to avoid alloreactive T cell responses and to control the reactivation of autoreactive memory T cells. However, lymphopenia associated with immunosuppression and T cell depletion can induce a paradoxical expansion of lymphocyte subsets under the influence of homeostatic proliferation. Homeostatic T cell proliferation is mainly driven by the IL-7/IL-7 receptor axis, a molecular pathway which is not affected by standard immune-suppressive drugs and, consequently, represents a novel potential target for immuno-modulatory strategies. In this review, we will discuss how homeostatic T cell proliferation can support autoimmunity recurrence after islet transplantation and how it can be targeted by new therapeutic approaches.

scholarly journals Engagement of the adhesion receptor CD22 triggers a potent stimulatory signal for B cells and blocking CD22/CD22L interactions impairs T-cell proliferation

Blood ◽  
1996 ◽  
Vol 87 (11) ◽  
pp. 4723-4730 ◽  
Author(s):  
J Tuscano ◽  
P Engel ◽  
TF Tedder ◽  
JH Kehrl
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
B Cell ◽  
B Lymphocyte ◽  
Tyrosine Phosphatase ◽  
Interleukin 2 ◽  
Culture Conditions ◽  
Cell Interactions ◽  
T Cell Proliferation ◽  
Downstream Signaling

The B-lymphocyte-restricted adhesion protein CD22 mediates sialic acid- dependent cell-cell interactions. Engagement of CD22 on B lymphocytes with a CD22 monoclonal antibody (MoAb) HB22.7 that blocks the binding of CD22 to its ligand(s) directly stimulated B-cell proliferation. In addition, the HB22.7 MoAb costimulated B-cell proliferation with either anti-IgM, interleukin-2 (IL-2), IL-4, or CD40 and triggered predominantly B-cell IgG secretion with IL-2. Even more striking levels of B-cell proliferation occurred with HB22.7 MoAb under culture conditions that enhanced B-B-cell interactions. In contrast, a nonblocking CD22 MoAb (CD22.5) poorly costimulated in similar experiments. The functional differences between the two antibodies likely result from differing abilities to trigger downstream signaling events as significant differences in CD22 tyrosine phosphorylation and the recruitment of the tyrosine kinase p53/56lyn and the tyrosine phosphatase SH-PTP1C were found. Besides their role in B-cell stimulation, CD22/CD22L interactions may also assist in regulating T- cell proliferation because inhibition of CD22-CD22L engagement with the HB22.7 MoAb impaired T-cell proliferation in a costimulatory assay. Thus, CD22/CD22L interactions result in stimulatory signals for both B and T lymphocytes.

scholarly journals APC dysfunction is correlated with defective suppression of T cell proliferation in human type 1 diabetes

2009 ◽  
Vol 130 (3) ◽  
pp. 272-279 ◽  
Author(s):  
Yulan Jin ◽  
Xueqin Chen ◽  
Robert Podolsky ◽  
Diane Hopkins ◽  
Levi H.C. Makala ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Type 1 Diabetes ◽  
T Cell ◽  
T Cell Proliferation ◽  
Human Type ◽  
Human Type 1 Diabetes
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