Imbalance of CD4+CD29+ and CD4+CD45RA+ T-helper cell subsets in peripheral blood of patients with severe atopic dermatitis

1993 ◽  
Vol 285 (3) ◽  
pp. 135-139 ◽  
Author(s):  
K. Jung ◽  
A. Bittrich ◽  
V. Klimmek ◽  
H. Schubert
2018 ◽  
Vol 180 (3) ◽  
pp. 586-596 ◽  
Author(s):  
M.A. McAleer ◽  
I. Jakasa ◽  
G. Hurault ◽  
P. Sarvari ◽  
W.H.I. McLean ◽  
...  

Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1388-1393 ◽  
Author(s):  
EJ Sjamsoedin-Visser ◽  
CJ Heijnen ◽  
BJ Zegers ◽  
JW Stoop

Abstract The capacity of the peripheral blood lymphocytes (PBL) to generate an antibody response in vitro T cell-dependent antigen ovalbumin was studied in 12 severe hemophilia patients who were otherwise in good health. PBL from four of 12 patients were not capable of generating such a response after stimulation in vitro, whereas all controls were normal. This negative plaque-forming cell (PFC) response coincided with the presence of antibodies directed toward human T-lymphotropic virus III/lymphadenopathy-associated virus (HTLV-III/LAV). Only one patient with antibodies against HTLV-III/LAV had a normal PFC response. The negative PFC response was not due to a deficient T helper cell activity, nor to an excessive T suppressor cell function. However, in the peripheral blood of these four patients, the presence of activated B cells that are refractory to antigen-specific T helper cell signals and secrete specific antibodies spontaneously could be demonstrated. Most of the patients showed a hyperimmunoglobulinemia. No correlation between the T4/T8 ratio and the level of the PFC response was demonstrable. From the data obtained in these investigations we raise the hypothesis that infection with HTLV-III/LAV in hemophilia patients will lead to in vivo (pre)activation of B cells that results in unresponsiveness or decreased response to antigen-specific signals.


2015 ◽  
Vol 18 (2) ◽  
pp. 206-215 ◽  
Author(s):  
Larry A. Harshyne ◽  
Brian J. Nasca ◽  
Lawrence C. Kenyon ◽  
David W. Andrews ◽  
D. Craig Hooper

Planta Medica ◽  
2019 ◽  
Vol 85 (07) ◽  
pp. 599-607 ◽  
Author(s):  
Baknoon Ham ◽  
Myungsuk Kim ◽  
Yang-Ju Son ◽  
Sungyul Chang ◽  
Sang Hoon Jung ◽  
...  

Abstract Pterocarpus santalinus has been traditionally used as a medicinal plant owing to its anti-inflammatory, anthelmintic, tonic, antihyperglycemic, and diaphoretic properties. We hypothesized that P. santalinus might have therapeutic potential in alleviating allergy and atopic dermatitis. Thus, we investigated the inhibitory effects of P. santalinus extract against allergic responses and 2,4-dinitrochlorobenzene-induced atopic dermatitis-like dorsal skin lesions using immunoglobulin E-sensitized rat basophilic leukemia-2H3 mast cells and NC/Nga mice. Degranulation and enzyme-linked immunosorbent assays were conducted to measure degranulation, proinflammatory cytokine levels, and prostaglandin E2 concentrations in immunoglobulin E/antigen-sensitized RBL-2H3 mast cells. The therapeutic efficacy of P. santalinus extract in 2,4-dinitrochlorobenzene-induced atopic dermatitis was evaluated through morphological, physiological, and immunological analysis. P. santalinus extract inhibited β-hexosaminidase and histamine release and reduced tumor necrosis factor-α, interleukin-4, and prostaglandin E2 secretion. Furthermore, P. santalinus extract suppressed atopic dermatitis-like skin lesions by regulating the serum levels of immunoglobulin E and immunoglobulin G2a, and messenger ribonucleic acid expression of T helper cell 1- and T helper cell 2-related mediators in the skin lesions. Histopathological analyses showed a decrease in epidermal thickness and intradermal inflammatory cell infiltration. These results suggested that P. santalinus extract might have beneficial effects in treating allergic and atopic dermatitis-like skin disorders.


2020 ◽  
Vol 11 ◽  
Author(s):  
Alansana Darboe ◽  
Carolyn M. Nielsen ◽  
Asia-Sophia Wolf ◽  
Jacob Wildfire ◽  
Ebrima Danso ◽  
...  

Innate lymphoid cell (ILC) lineages mirror those of CD4+ T helper cell subsets, producing type 1, 2 and 3 cytokines respectively. Studies in adult human populations have shown contributions of non-cytotoxic ILC to immune regulation or pathogenesis in a wide range of diseases and have prompted investigations of potential functional redundancy between ILC and T helper cell compartments in neonates and children. To investigate the potential for ILC to contribute to immune responses across the human lifespan, we examined the numbers and frequencies of peripheral blood ILC subsets in a cohort of Gambians aged between 5 and 73 years of age. ILC2 were the most abundant peripheral blood ILC subset in this Gambian cohort, while ILC1 were the rarest at all ages. Moreover, the frequency of ILC1s (as a proportion of all lymphocytes) was remarkably stable over the life course whereas ILC3 cell frequencies and absolute numbers declined steadily across the life course and ILC2 frequencies and absolute numbers declined from childhood until the age of approx. 30 years of age. Age-related reductions in ILC2 cell numbers appeared to be partially offset by increasing numbers of total and GATA3+ central memory (CD45RA-CCR7+) CD4+ T cells, although there was also a gradual decline in numbers of total and GATA3+ effector memory (CD45RA-CCR7-) CD4+ T cells. Despite reduced overall abundance of ILC2 cells, we observed a coincident increase in the proportion of CD117+ ILC2, indicating potential for age-related adaptation of these cells in childhood and early adulthood. While both CD117+ and CD117- ILC2 cells produced IL-13, these responses occurred predominantly within CD117- cells. Furthermore, comparison of ILC frequencies between aged-matched Gambian and UK young adults (25–29 years) revealed an overall higher proportion of ILC1 and ILC2, but not ILC3 in Gambians. Thus, these data indicate ongoing age-related changes in ILC2 cells throughout life, which retain the capacity to differentiate into potent type 2 cytokine producing cells, consistent with an ongoing role in immune modulation.


2013 ◽  
Vol 109 (01) ◽  
pp. 112-117 ◽  
Author(s):  
Intawat Nookaew ◽  
Hans Wadenvik ◽  
Bob Olsson ◽  
Margareta Jernås

SummaryPrimary immune thrombocytopenia (ITP) is an autoimmune disease characterised by premature platelet destruction in spleen, liver and bone marrow and a diminished production of platelets. T-cells are important in all forms of autoimmunity including ITP; however, very little is known about T-cells in organs where platelets are destroyed. Our aim was to investigate differences in gene expression in peripheral blood-derived T-cells and bone marrow-derived T-cells between ITP patients and controls. T-cells and subsequent RNA were isolated from blood and bone marrow from chronic ITP patients and healthy controls followed by DNA microarray analysis. There were 1554 differentially expressed genes in peripheral blood-derived T-cells and 976 in bone marrow-derived T-cells between ITP patients and controls and three genes were verified with real-time PCR. Using Gene Ontology functional enrichment analysis we found that genes involved in growth, development, migration, chemotaxis, adhesion and apoptosis were enriched in bone marrow-derived T-cells in ITP. Immune-related genes involved in T-helper cell differentiation, T-cell chemotaxis, migration, immunoglobulin-mediated immune response and classical and alternative pathway complement activation were also enriched in bone marrow-derived T-cells in ITP. Only 213 T-cell genes were differentially expressed in both blood and bone marrow between ITP patients and controls. In conclusion, our findings show that genes involved in major pathophysiologic pathways in ITP such as T-helper cell differentiation, autoantibody response and complement activation are altered in bone marrow-derived T-cells in ITP patients compared with controls. This further supports the concept that bone marrow is an important compartment in ITP.


2002 ◽  
Vol 8 (6) ◽  
pp. 452-458 ◽  
Author(s):  
W Royal ◽  
S Gartner ◽  
C D Gajewski

Treatment with interferon (IFN)-β1a has been associated with decreased disease activity in patients with multiple sclerosis (MS). In several biological systems, type I IFNs and retinoids have been demonstrated to have synergistic effects. In these studies, we measured blood and cerebrospinal fluid (CSF) retinol levels and naïve and memory T-helper cell subset percentages in samples from a group of patients with MS. We also examined retinol receptor expression in peripheral blood cells from MS patients with or without a history of prior treatment with IFN-β1a. The mean plasma retinol level for untreated relapsing-remitting (RR) MS patients was lower than for patients with noninflammatory neurological disease. Among IFN-β1a-treated RR patients, mean levels were slightly higher than for RR patients not on treatment. Lower plasma retinol levels among the MS patients studied were associated with higher CSF retinol index measurements - a measure that was calculated to correct for nonspecific leakage of retinol from blood into CSF. For the MS samples examined, there was a borderline statistically significant direct correlation between CSF retinol index measurements and CSF memory T-helper cell percentages. Examination of peripheral blood from untreated RR patients for retinoid receptor mRNA expression revealed the expression of the retinoic acid receptor (RAR)-α, RAR-γ, and retinoic X receptor (RXR)-α receptor subtypes. For RR patients on IFN-β1a therapy, expression of the same RAR subtypes was noted as well as expression of RXR-βand RXR-γ. These studies suggest an association between plasma retinol levels and clinical disease activity in patients with MS and that treatment with IFN-β1a may be associated with activation of specific retinoid receptor subtypes.


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