Clonally expanded γδ T cells protect against Staphylococcus aureus skin reinfection

IL-17–producing γδ T cells protect against Clostridium difficile infection

“…However, combined stimulation resulted in markedly increased IL-17 production, a finding consistent with recent studies suggesting that TCR signaling may enhance activation through upregulated expression of cytokine receptors, effectively licensing cells for high-level activation (60,77,99). The TCR may also contribute to the recently identified capacity for γδ cells to develop a memory phenotype and expand in response to reinfection when they often have the capacity to coproduce IL-17A and TNF-α (100,101) The contribution of TCR signaling to IL-17 release prompted us to investigate TCR gene usage by these cells. We found that the vast majority expressed the γ chains Trgv6 or Trgv2 in association with the δ chain Trdv4.…”

Inhibition of protective immunity against Staphylococcus aureus infection by MHC-restricted immunodominance is overcome by vaccination

“…However, in a mouse model of S. aureus peritonitis, memory T H 1 cells were protective (14). A recent study confirmed that C57BL/6 mice were not protected against secondary SSTI (16); however, IL-1 −/− C57BL/6 mice were partially protected against secondary infection in an antibody-independent manner due to clonal expansion of memory  T cells. Together, integration of each of the distinct mouse models of recurrent infection suggests that, depending on the site of infection and the genetic background of the mice studied, protective immunity depends on a combination of T H 1-, T H 17-, and  T cell-mediated mechanisms in concert with protective antibody responses.…”

Staphylococcus aureus toxin suppresses antigen-specific T cell responses

“…Although the molecular pathogenesis of recurrent infection is poorly understood, host and pathogen factors contribute to susceptibility. Humans harboring defects in neutrophil and T cell function and IL-17 signaling present with recurrent infection (11), an observation corroborated by mouse models that demonstrate the importance of innate and adaptive immunity (12)(13)(14)(15)(16). S. aureus thwarts immunity through an array of virulence factors (17) including α-toxin (Hla), a pore-forming cytotoxin that contributes to superficial and invasive disease (18)(19)(20) and perturbs host immunity during skin infection (21) and recurrent disease (22).…”