The Effector Component of the Cytotoxic T-Lymphocyte Response Has a Biphasic Pattern after Burn Injury

Hunt, John P.; Hunter, Christopher L.; Brownstein, Michelle R.; Giannopoulos, Athina; Hultman, C. Scott; deSerres, Suzan; Bracey, Lyndie; Frelinger, Jeffrey A.; Meyer, Anthony A.

doi:10.1006/jsre.1998.5488

Cited by 39 publications

(16 citation statements)

References 21 publications

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“…To characterize T cell function following burn injury, we used a well-described scald burn injury in mice (26,28,31). In support of our previous findings (31), we found that there is consistent suppression in T cell proliferative response to anti-CD3 and Splenocytes from burn mice demonstrate increased pro-and anti-inflammatory cytokine secretion after activation in vitro.…”

Section: Cd8 ϩ T Cell Response To Burn Injury Is Dynamic and Time Depsupporting

confidence: 79%

“…Third, the majority of lymphocyte studies focuses solely on the early response to burn injury (Ͻ10 days) or involves another insult (such as cecal ligation and puncture) within a week of burn injury and thus may have missed an important characteristic of the T cell response to injury. Finally, of particular relevance to burn injury is the effect of enhanced memory-like CD8 ϩ T cell activity on allograft rejection (29,31). We have demonstrated that the cycling memory-like CD8 ϩ T cells which arise late after burn injury are costimulation independent and hyperresponsive to antigenic stimuli, including alloantigens.…”

Section: Discussionmentioning

confidence: 96%

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Lymphopenia-Induced Homeostatic Proliferation of CD8+ T Cells Is a Mechanism for Effective Allogeneic Skin Graft Rejection following Burn Injury

Maile

Barnes²,

Nielsen³

et al. 2006

The Journal of Immunology

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Burn patients are immunocompromised yet paradoxically are able to effectively reject allogeneic skin grafts. Failure to close a massive burn wound leads to sepsis and multiple system organ failure. Immune suppression early (3 days) after burn injury is associated with glucocorticoid-mediated T cell apoptosis and anti-inflammatory cytokine responses. Using a mouse model of burn injury, we show CD8+ T cell hyperresponsiveness late (14 days) after burn injury. This is associated with a CD8+ T cell pro- and anti-inflammatory cytokine secretion profile, peripheral lymphopenia, and accumulation of a rapidly cycling, hyperresponsive memory-like CD8+CD44+ IL-7R− T cells which do not require costimulation for effective Ag response. Adoptive transfer of allospecific CD8+ T cells purified 14 days postburn results in enhanced allogeneic skin graft rejection in unburned recipient mice. Chemical blockade of glucocorticoid-induced lymphocyte apoptosis early after burn injury abolishes both the late homeostatic accumulation of CD8+ memory-like T cells and the associated enhanced proinflammatory CD8+ T cell response, but not the late enhanced CD8+ anti-inflammatory response. These data suggest a mechanism for the dynamic CD8+ T cell response following injury involving an interaction between activation, apoptosis, and cellular regeneration with broad clinical implications for allogeneic skin grafting and sepsis.

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Section: Cd8 ϩ T Cell Response To Burn Injury Is Dynamic and Time Depsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 96%

Lymphopenia-Induced Homeostatic Proliferation of CD8+ T Cells Is a Mechanism for Effective Allogeneic Skin Graft Rejection following Burn Injury

Maile

Barnes²,

Nielsen³

et al. 2006

The Journal of Immunology

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“…One paradigm of T cell response to burn injury suggests that CD4 + T cells are pro-inflammatory and produce Th1 cytokines in response to the injury, while CD8 + T cells are counter-inflammatory and regulatory in nature [76]. Consistent with this paradigm, some studies demonstrate a Th2 (Tc2) phenotype cytokine secretion by CD8 + T cells with a decreased antigen-specific proliferative and cytolytic response [77,78]. However, other groups have evidence of CD8 + T cells producing Th1 (Tc1) cytokines similar to their CD4 + T cell counterparts following burn [79].…”

Section: Adaptive Immune Response Following Injurymentioning

confidence: 94%

Sex differences and estrogen modulation of the cellular immune response after injury

Bird¹,

Karavitis²,

Kovacs³

2008

Cellular Immunology

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Cell-mediated immunity is extremely important for resolution of infection and for proper healing from injury. However, the cellular immune response is dysregulated following injuries such as burn and hemorrhage. Sex hormones are known to regulate immunity, and a well-documented dichotomy exists in the immune response to injury between the sexes. This disparity is caused by differences in immune cell activation, infiltration, and cytokine production during and after injury. Estrogen and testosterone can positively or negatively regulate the cellular immune response either by aiding in resolution or by compounding the morbidity and mortality. It is apparent that the hormonal dysregulation is dependent not only on the type of injury sustained but also the amount of circulating hormones. Therefore, it may be possible to design sex-specific therapies to improve immunological function and patient outcome.

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“…A multitude of immunological alterations have been reported to occur both in burned patients and in animal models of burn injury. These alterations include depressed NK cell activity (5,23,45), decreased T-cell proliferation, and altered cytotoxic T-lymphocyte activities (20,21,47). Additionally, impairments in macrophage and neutrophil functions have been reported (9,25,40).…”

mentioning

confidence: 99%

Stimulation of Hematopoiesis by the Fms-Like Tyrosine Kinase 3 Ligand Restores Bacterial Induction of Th1 Cytokines in Thermally Injured Mice

Toliver‐Kinsky

Chen²,

Herndon

et al. 2003

Infect Immun

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The Effector Component of the Cytotoxic T-Lymphocyte Response Has a Biphasic Pattern after Burn Injury

Cited by 39 publications

References 21 publications

Lymphopenia-Induced Homeostatic Proliferation of CD8+ T Cells Is a Mechanism for Effective Allogeneic Skin Graft Rejection following Burn Injury

Lymphopenia-Induced Homeostatic Proliferation of CD8+ T Cells Is a Mechanism for Effective Allogeneic Skin Graft Rejection following Burn Injury

Sex differences and estrogen modulation of the cellular immune response after injury

Stimulation of Hematopoiesis by the Fms-Like Tyrosine Kinase 3 Ligand Restores Bacterial Induction of Th1 Cytokines in Thermally Injured Mice

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