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a novel endogenous trigger for autoimmune diabetes and an in vivo role for granzyme A in maintaining immune tolerance.
this study shows that gzmA and gzmB partly regulate local inflammation during early pneumonia but eventually play an insignificant role during pneumosepsis by the common human pathogen Klebsiella pneumoniae
Granzyme A does not have a crucial role in vivo in the protective response to tuberculosis.
The results, in susceptible B6 mice for GzmB and in resistant 129/Sv mice for GzmA and/or the GzmB cluster, point to granzyme-mediated host defense regulation in the liver in experimental visceral leishmaniasis.
Estrogen increases the extracellular expression and interleukin (IL)-12 (show IL12A Proteins)-induced activity of a critical member of serine protease (show F2 Proteins) family granzyme A.
functional divergence between human and mouse granzyme A
Regulated secretion of granzyme A and cytotoxic killing was enhanced and correlated with increased vesicle-associated membrane protein 7 (show VAMP7 Proteins) availability.
GzmA deficiency in filarial infection is linked with reduced inflammation and a trend toward increased alternatively activated macrophages.
granzyme A- and B-cluster deficiency delays the acute progression of pneumovirus disease by reducing alveolar injury.
the genes for perforin (show PRF1 Proteins), the three major T cell granzymes (A-C) and IFN-gamma (show IFNG Proteins) are differentially expressed during primary activation of naive CD8 (show CD8A Proteins)(+) T cells, kinetically and at the single-cell level
granzyme A in human platelets increases with aging
GzmA plays an unfavorable role in host defense during pneumococcal pneumonia by a mechanism that does not depend on natural killer cells.
Carbamate pesticides significantly reduced the intracellular levels of perforin (show PRF1 Proteins), GrA (show NR3C1 Proteins), GrB, Gr3 (show PRLHR Proteins)/K, and GRN (show GRN Proteins) in NK-92CI cells.
Our results suggest that granzyme A could be considered another biomarker of TB, that can be used, other than IFN-gamma (show IFNG Proteins), to discriminate between patients with active TB and LTBI subjects
Delivered into parasite infected cells by granulysin (show GNLY Proteins) and perforin (show PRF1 Proteins), granzymes generate superoxide and inactivate oxidative defense enzymes to kill the parasite.
Taken together, the authors verified that histone H3 (show HIST3H3 Proteins) is a real substrate for GzmA in vivo in the Raji cells treated by staurosporin.
Results reveal enhanced intra- and extracellular expression of gzmA and B in patients with pulmonary TB, suggesting that gzms are part of the host response to tuberculosis.
Levels of GZMA and ITGAE (show ITGAE Proteins) mRNAs in colon tissues can identify patients with UC who are most likely to benefit from etrolizumab; expression levels decrease with etrolizumab administration in biomarker(high) patients.
GzmA and GzmB expressing cells in the airways and lung parenchyma was higher in subjects who died from asthma
GZMA, GBP5 and CD64 (show FCGR1A Proteins) genes show promise as a rapid diagnostic markers separating tuberculosis from other pulmonary diseases.
Cytolytic T lymphocytes (CTL) and natural killer (NK) cells share the remarkable ability to recognize, bind, and lyse specific target cells. They are thought to protect their host by lysing cells bearing on their surface 'nonself' antigens, usually peptides or proteins resulting from infection by intracellular pathogens. The protein described here is a T cell- and natural killer cell-specific serine protease that may function as a common component necessary for lysis of target cells by cytotoxic T lymphocytes and natural killer cells.
, Granzyme A
, BLT esterase
, H factor
, Hanukah factor
, autocrine thymic lymphoma granzyme-like serine protease
, serine esterase 1
, t cell-specific serine protease 1
, CTL tryptase
, Granzyme A (Cytotoxic T-lymphocyte-associated serine esterase-3; Hanukah factor serine protease)
, cytotoxic T-lymphocyte proteinase 1
, h factor