Comparative analysis of lymphocyte activation marker expression and cytokine secretion profile in stimulated human peripheral blood mononuclear cell cultures: an in vitro model to monitor cellular immune function

Reddy, Manjula; Eirikis, Edward; Davis, Cuc; Davis, Hugh M.; Prabhakar, Uma

doi:10.1016/j.jim.2004.07.006

Cited by 261 publications

(233 citation statements)

References 31 publications

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“…T-cell activation (16)(17)(18), and have previously shown that its expression is low in CD4 + and CD8 + T cells during the acute phase of KD (20,28,29). This data was further corroborated by another research group, which observed that the number of HLA-DR + CD8 + T cells does not increase during the acute phase of KD (30).…”

Section: Discussionsupporting

confidence: 52%

“…Autopsy studies of children with KD who died during the acute phase clearly indicate that CD4 + and CD8 + T cells participate in the transmural infiltration of the coronary arterial wall (14). Notably, human leukocyte antigen-DR (HLA-DR), a cell-surface glycoprotein encoded by the HLA-DR region of the major histocompatibility complex (15), is a known marker of T-cell activation (16)(17)(18), but the function of this antigen on the different T-cell populations during KD is unknown. In this study, we have investigated the relationship between HLA-DR expression on peripheral CD4 + and CD8 + T cells, and thus the activation of these cells, and the response to IVIG treatment in children with KD.…”

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confidence: 99%

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Relationship between T-cell HLA-DR expression and intravenous immunoglobulin treatment response in Kawasaki disease

et al. 2015

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Background: Kawasaki disease (KD) is an acute febrile illness associated with the development of vasculitis. Administration of intravenous immunoglobulin (IVIG) is the standard treatment for KD. However, IVIG treatment is not effective in approximately 15% of children with KD. Some reports have presented evidence of immunological responses in IVIG-resistant KD patients.We assessed the possibility that T-cell activation is a contributing mechanism underlying this phenomenon.

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Section: Discussionsupporting

confidence: 52%

mentioning

confidence: 99%

Relationship between T-cell HLA-DR expression and intravenous immunoglobulin treatment response in Kawasaki disease

et al. 2015

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“…The increase in expression were analyzed after 24 h, the time required to induce these activation markers (40), before shifts occurred from the original naïve phenotype and within the memory subsets. Interestingly, the preferential costimulatory effect could be observed even at longer times after initiation of the signals.…”

Section: Kinetics Of Early Signaling Events In T-cell Activation Depementioning

confidence: 99%

Complementary costimulation of human T-cell subpopulations by cluster of differentiation 28 (CD28) and CD81

Sagi¹,

Landrigan

Levy³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Cluster of differentiation 81 (CD81) is a widely expressed tetraspanin molecule that physically associates with CD4 and CD8 on the surface of human T cells. Coengagement of CD81 and CD3 results in the activation and proliferation of T cells. CD81 also costimulated mouse T cells that lack CD28, suggesting either a redundant or a different mechanism of action. Here we show that CD81 and CD28 have a preference for different subsets of T cells: Primary human naïve T cells are better costimulated by CD81, whereas the memory T-cell subsets and Tregs are better costimulated by CD28. The more efficient activation of naïve T cells by CD81 was due to prolonged signal transduction compared with that by CD28. We found that IL-6 played a role in the activation of the naïve T-cell subset by CD81. Combined costimulation through both CD28 and CD81 resulted in an additive effect on Tcell activation. Thus, these two costimulatory molecules complement each other both in the strength of signal transduction and in T-cell subset inclusions. Costimulation via CD81 might be useful for expansion of T cells for adoptive immunotherapy to allow the inclusion of naïve T cells with their broad repertoire.

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“…INF-g, IL-1, TNF-a and IL-6 are also instrumental in mounting an effective inflammatory response against infection. IFN-g is a pivotal cytokine initiating antimicrobial Th1 responses and plays a key role in activating macrophages and natural killer cells, whereas IL-1, IL-6 and TNF-a acting together are key to leukocyte transmigration, stimulating macrophage phagocytosis and evoking acute phase responses (Bendtzen, 1988;Urbaschek and Urbaschek, 1990;Van der Meide and Schellekens, 1996;Reddy et al, 2004). Splenocytes showed a profound inability to produce these key proliferative/inflammatory cytokines on mitogen 98.5 ± 0.3 a 94.7 ± 0.6 b 95.0 ± 1.7 b 92.5 ± 0.8 a 71.3 ± 3.0 b 91.7 ± 0.9 a % OX12+CD80+ 0.7 ± 0.1 a 1.5 ± 0.5 a,b 2.6 ± 1.1 b 2.8 ± 0.4 3.9 ± 0.7 2.5 ± 0.3 CD3+(% of total cells) 70.…”

Section: Hypo-responsive and Anergic State Of Splenocytesmentioning

confidence: 99%

Prophylactic ciprofloxacin treatment prevented high mortality, and modified systemic and intestinal immune function in tumour-bearing rats receiving dose-intensive CPT-11 chemotherapy

et al. 2009

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Infectious complications are a major cause of morbidity and mortality from dose-intensive cancer chemotherapy. In spite of the importance of intestinal bacteria translocation in these infections, information about the effect of high-dose chemotherapy on gut mucosal immunity is minimal. We studied prophylactic ciprofloxacin (Cipro) treatment on irinotecan (CPT-11) toxicity and host immunity in rats bearing Ward colon tumour. Cipro abolished chemotherapy-related mortality, which was 45% in animals that were not treated with Cipro. Although Cipro reduced body weight loss and muscle wasting, it was unable to prevent severe late-onset diarrhoea. Seven days after CPT-11, splenocytes were unable to proliferate (stimulation index ¼ 0.10 ± 0.02) and produce proliferative and inflammatory cytokines (i.e., Interleukin (IL)-2, interferon-g (IFN-g), tumour necrosis factor-a (TNF-a) IL-1b, IL-6) on mitogen stimulation in vitro (Po0.05 vs controls), whereas mesenteric lymph node (MLN) cells showed a hyper-proliferative response and a hyper-production of pro-inflammatory cytokines on mitogen stimulation. This suggests compartmentalised effects by CPT-11 chemotherapy on systemic and intestinal immunity. Cipro normalised the hyper-responsiveness of MLN cells, and in the spleen, it partially restored the proliferative response and normalised depressed production of IL-1b and IL-6. Taken together, Cipro prevented infectious challenges associated with immune hypo-responsiveness in systemic immune compartments, and it may also alleviate excessive pro-inflammatory responses mediating local gut injury.

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Comparative analysis of lymphocyte activation marker expression and cytokine secretion profile in stimulated human peripheral blood mononuclear cell cultures: an in vitro model to monitor cellular immune function

Cited by 261 publications

References 31 publications

Relationship between T-cell HLA-DR expression and intravenous immunoglobulin treatment response in Kawasaki disease

Relationship between T-cell HLA-DR expression and intravenous immunoglobulin treatment response in Kawasaki disease

Complementary costimulation of human T-cell subpopulations by cluster of differentiation 28 (CD28) and CD81

Prophylactic ciprofloxacin treatment prevented high mortality, and modified systemic and intestinal immune function in tumour-bearing rats receiving dose-intensive CPT-11 chemotherapy

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