Effects of the ablation of the left cerebral cortex on T-cell number and cell-medaited responses in the mouse

1980 ◽  
Vol 2 (3) ◽  
pp. 156 ◽  
Author(s):  
G. Renoux ◽  
K. Bizière ◽  
M. Renoux ◽  
L. Gyenes ◽  
D. Degenne ◽  
...  
Keyword(s):  
T Cell ◽  
Blood ◽  
2019 ◽  
Vol 133 (24) ◽  
pp. 2586-2596 ◽  
Author(s):  
Giuliana Giardino ◽  
Nesrine Radwan ◽  
Patra Koletsi ◽  
Deborah M. Morrogh ◽  
Stuart Adams ◽  
...  

Abstract DiGeorge syndrome (DGS) is a primary immunodeficiency characterized by various degrees of T-cell deficiency. In partial DGS (pDGS), other risk factors could predispose to recurrent infections, autoimmunity, and allergy. The aim of this study was to assess the effect of different factors in the development of infections, autoimmunity, and/or allergy in patients with pDGS. We studied 467 pDGS patients in follow-up at Great Ormond Street Hospital. Using a multivariate approach, we observed that palatal anomalies represent a risk factor for the development of recurrent otitis media with effusion. Gastroesophageal reflux/dysphagia and asthma/rhinitis represent a risk factor for the development of recurrent upper respiratory tract infections. Allergy and autoimmunity were associated with persistently low immunoglobulin M levels and lymphopenia, respectively. Patients with autoimmunity showed lower levels of CD3+, CD3+CD4+, and naïve CD4+CD45RA+CD27+ T lymphocytes compared with pDGS patients without autoimmunity. We also observed that the physiological age-related decline of the T-cell number was slower in pDGS patients compared with age-matched controls. The age-related recovery of the T-cell number depended on a homeostatic peripheral proliferation of T cells, as suggested by an accelerated decline of the naïve T lymphocytes in pDGS as well as a more skewed T-cell repertoire in older pDGS patients. These evidences suggest that premature CD4+ T-cell aging and lymphopenia induced spontaneous peripheral T-cell proliferation might contribute to the pathogenesis of autoimmunity in patients with pDGS. Infections in these patients represent, in most of the cases, a complication of anatomical or gastroenterological anomalies rather than a feature of the underlying immunodeficiency.


1989 ◽  
Vol 13 (4) ◽  
pp. 392
Author(s):  
B. Fedecka-Bruner ◽  
J. Desveaux-Chabrol ◽  
F. Dieterlen-Liévre

Oral Oncology ◽  
2017 ◽  
Vol 67 ◽  
pp. 183-191 ◽  
Author(s):  
Nadège Kindt ◽  
Géraldine Descamps ◽  
Imelda Seminerio ◽  
Justine Bellier ◽  
Jérôme R. Lechien ◽  
...  

Author(s):  
Elisa Maritza Linares Guerra ◽  
Sergio Santana Porbén

Blood ◽  
2002 ◽  
Vol 99 (11) ◽  
pp. 4225-4227 ◽  
Author(s):  
JoAnn C. Castelli ◽  
Steven G. Deeks ◽  
Stephen Shiboski ◽  
Jay A. Levy

During chronic HIV infection, asymptomatic individuals demonstrate a strong CD8+ cell noncytotoxic antiviral response (CNAR). With the onset of symptoms or reduction in CD4+ cell counts, CNAR decreases. Presently, it is recommended that infected individuals receive antiretroviral therapy if CD4+ cell counts fall below 350 cells/μL. To determine whether CNAR lends support to this recommendation for initiation of antiretroviral treatment, we examined CNAR in 20 healthy, untreated, HIV-infected men exhibiting a range of CD4+ cell numbers. Our results indicate that the asymptomatic untreated HIV-infected individuals with less than 300 CD4+ cells/μL had a significantly lower CNAR than those with higher CD4+ cell counts. These data on CNAR in untreated, healthy, HIV-infected individuals support the current recommendation for when to initiate antiretroviral therapy.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4653-4653
Author(s):  
James E Talmadge ◽  
Elizabeth Reed ◽  
Kenneth Cowan ◽  
Dmitry Gabrilovich ◽  
Phyllis Warkentin ◽  
...  

Abstract Myeloid derived suppressor cells (MDSCs) have been reported to be expanded in cancer patients, following growth factor administration and after chemotherapy. These cells have been associated with a loss of T-cell number and function and provide one mechanism of immune evasion. We examined the effect of dose dense chemotherapy on immune phenotypes and function in patients with breast cancers 4 cms or larger and/or four or more involved nodes. The adjuvant therapy was dose-dense doxorubicin, cyclophosphamide (AC) followed by paclitaxel (P), then 33 doses of radiation (R). Blood samples were obtained and studied prior to therapy, 1 week post AC and 1, 15 and 21 weeks post P and then 3, 6 and 12 months later. Flow cytometric analyses of cellular phenotypes were done on these blood specimens and compared to the levels prior to therapeutic intervention and to normal age and sex matched donors. Twenty-three pts have been followed a median of 29 months (range 5.5–50.5 months) from study entry. Two patients relapsed 8 and 23 months after diagnosis. T-cell CD-4 numbers declined following AC from an average of 4.9±0.5 ×106/ml to 1.7±0.3×106/ml, but increased to an average of 2.7± 0.3 × 106/ml, 21 weeks after P or 12 weeks after R. In this study the MDSCs were defined as Lin- (CD3, CD19, CD14 and CD13), HLA-DR- and CD33+. The numbers of MDSCs, which in normal donors were 0.62±0.16×106/ml and in the cancer patients at diagnosis were 11.8±9.6×106/ml increased to 58.4±25.9×106/ml 15 weeks after R. They remained significantly elevated through one year after diagnosis when they were 27.3±12.3×106/ml. The majority of the MDSCs had a high side scatter and forward scatter by flow analysis suggesting a granulocytic commitment rather than a monocytic commitment. The increase in MDSC numbers was apparently associated with R as the numbers of MDSCs were not significantly increased by AC (15.7±13.5×106/ml) or P (10.9±6×106/ml) one week following completion of each cycle of dose dense therapy. In association with the increase in MDSCs there was a significant decrease in PHA proliferation by the peripherial blood mononuclear cells (MNCs) and suppressive activity by irradiated MNC for allergenic lymphocytes.


2006 ◽  
Vol 242 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Kenneth S. Knox ◽  
Richard B. Day ◽  
Lisa M. Kohli ◽  
Chadi A. Hage ◽  
Homer L. Twigg

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