Atopic asthma: differential activation phenotypes among memory T helper cells

Lara-Marquez, Maria Luz; Moan, M. J.; Cartwright, Sara; Listman, James A.; Israel, Elliot; Perkins, David L.; Christiani, David C.

doi:10.1046/j.1365-2222.2001.01146.x

Cited by 15 publications

(10 citation statements)

References 25 publications

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“…Our study demonstrates that EM CD4 T cells depend on ICOS costimulation for long-term survival, suggesting that ICOS-blockade might reduce the survival of EM CD4 T cell populations and enhancing ICOS costimulation might augment the survival of these populations. Understanding how ICOS regulates the development and the survival of EM CD4 cells may enhance novel vaccination strategies aimed at inducing protective EM CD4 T cells [41], [44] and regulatory strategies to control CD4 responses in diseases such as atopic asthma that are exacerbated by EM CD4 T cells [47], [48], [49], [50], [51], [52].…”

Section: Discussionmentioning

confidence: 99%

Protective Effector Memory CD4 T Cells Depend on ICOS for Survival

et al. 2011

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Memory CD4 T cells play a vital role in protection against re-infection by pathogens as diverse as helminthes or influenza viruses. Inducible costimulator (ICOS) is highly expressed on memory CD4 T cells and has been shown to augment proliferation and survival of activated CD4 T cells. However, the role of ICOS costimulation on the development and maintenance of memory CD4 T cells remains controversial. Herein, we describe a significant defect in the number of effector memory (EM) phenotype cells in ICOS−/− and ICOSL−/− mice that becomes progressively more dramatic as the mice age. This decrease was not due to a defect in the homeostatic proliferation of EM phenotype CD4 T cells in ICOS−/− or ICOSL−/− mice. To determine whether ICOS regulated the development or survival of EM CD4 T cells, we utilized an adoptive transfer model. We found no defect in development of EM CD4 T cells, but long-term survival of ICOS−/− EM CD4 T cells was significantly compromised compared to wild-type cells. The defect in survival was specific to EM cells as the central memory (CM) ICOS−/− CD4 T cells persisted as well as wild type cells. To determine the physiological consequences of a specific defect in EM CD4 T cells, wild-type and ICOS−/− mice were infected with influenza virus. ICOS−/− mice developed significantly fewer influenza-specific EM CD4 T cells and were more susceptible to re-infection than wild-type mice. Collectively, our findings demonstrate a role for ICOS costimulation in the maintenance of EM but not CM CD4 T cells.

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Section: Discussionmentioning

confidence: 99%

Protective Effector Memory CD4 T Cells Depend on ICOS for Survival

et al. 2011

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“…44 Moreover, the circulating blood in healthy children after exercise reflected a progression of T cells from naive to memory, also typically found in atopic participants and in participants with asthma. 41 Although we did not measure intracellular cytokines and could not, therefore, gauge the shift in T helper 1 versus T helper 2 lymphocytes, the change in T helper cell numbers in general indicate the possibility that an altered balance of the pattern of these key cytokine-producing lymphocytes might have occurred in circulation even in healthy children after exercise.…”

Section: Figurementioning

confidence: 96%

“…Memory T helper cells (CD4+ CD45RO+) have previously been shown to be increased in patients with asthma and after antigen challenge. 41 Moreover, recent work shows that memory T cells originating in the circulation can migrate to the airways and cause bronchoconstriction even in the absence of eosinophils. 42 Thus, the lower level of the memory T helper cell with upregulated adhesion molecule expression (CD4+ CD29+ CD45RO+) may indicate migration of this cell to areas of inflammation in the patients with asthma, such as the lung.…”

Section: Figurementioning

confidence: 99%

Do circulating leucocytes and lymphocyte subtypes increase in response to brief exercise in children with and without asthma?

et al. 2006

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Background: Exercise can alter health in children in both beneficial (eg reduced long-term risk of atherosclerosis) and adverse (eg exercise-induced asthma) ways. The mechanisms linking exercise and health are not known, but may rest, partly, on the ability of exercise to increase circulating immune cells. Little is known about the effect of brief exercise, more reflective of naturally occurring patterns of physical activity in children, on immune cell responses. Objectives: To determine whether (1) a 6-min bout of exercise can increase circulating inflammatory cells in healthy children and (2) the effect of brief exercise is greater in children with a history of asthma. Methods: Children with mild-moderate persistent asthma and age-matched controls (n = 14 in each group, mean age 13.6 years) performed a 6-min bout of cycle-ergometer exercise. Spirometry was performed at baseline and after exercise. Blood was drawn before and after exercise, leucocytes were quantified and key lymphocyte cell surface markers were assessed by flow cytometry. Results: Exercise decreased spirometry only in children with asthma, but increased (p,0.001) most types of leucocytes (eg lymphocytes (controls, mean (SD) 1210 (208) cells/ml; children with asthma, 1119 (147) cells/ml) and eosinophils (controls, 104 (22) cells/ml; children with asthma, 88 (20) cells/ml)) to the same degree in both groups. Similarly, exercise increased T helper cells (controls, 248 (60) cells/ml; children with asthma, 232 (53) cells/ml) and most other lymphocyte subtypes tested. By contrast, although basophils (16 (5) cells/ml) and CD4+ CD45RO+ RA+ lymphocytes (19 (4) cells/ml) increased in controls, no increase in these cell types was found in children with asthma. Conclusions: Exercise increased many circulating inflammatory cells in both children with asthma and controls. Circulating inflammatory cells did increase in children with asthma, but not to a greater degree than in controls. In fact, basophils and T helper lymphocyte memory transition cells did not increase in children with asthma, whereas they did increase in controls. Even brief exercise in children and adolescents robustly mobilises circulating immune cells.

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“…Only activated/memory (CD45RO + ) CD4 + T cells are the effector cells infiltrating into inflammatory tissues upon antigen exposure (13). Even then, it remains unclear whether AdIκBαM could suppress the immune response in memory Th (CD4 + CD45RO + ) cells, and what this potentially implicates for immunotherapy of asthma.…”

mentioning

confidence: 99%

Selective blockade of NF‐κB by novel mutated IκBα suppresses CD3/CD28‐induced activation of memory CD4⁺ T cells in asthma

Zhou

Zhang

et al. 2007

Allergy

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Atopic asthma: differential activation phenotypes among memory T helper cells

Cited by 15 publications

References 25 publications

Protective Effector Memory CD4 T Cells Depend on ICOS for Survival

Protective Effector Memory CD4 T Cells Depend on ICOS for Survival

Do circulating leucocytes and lymphocyte subtypes increase in response to brief exercise in children with and without asthma?

Selective blockade of NF‐κB by novel mutated IκBα suppresses CD3/CD28‐induced activation of memory CD4⁺ T cells in asthma

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Atopic asthma: differential activation phenotypes among memory T helper cells

Cited by 15 publications

References 25 publications

Protective Effector Memory CD4 T Cells Depend on ICOS for Survival

Protective Effector Memory CD4 T Cells Depend on ICOS for Survival

Do circulating leucocytes and lymphocyte subtypes increase in response to brief exercise in children with and without asthma?

Selective blockade of NF‐κB by novel mutated IκBα suppresses CD3/CD28‐induced activation of memory CD4+ T cells in asthma

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Selective blockade of NF‐κB by novel mutated IκBα suppresses CD3/CD28‐induced activation of memory CD4⁺ T cells in asthma