Among the 15 HLA-DRB1, 3 DRB3, 9 DQA1, 15 DQB1, and 19 DPB1 alleles examined, none were found to be significantly associated with KS, except for an increased frequency of HLA-DRB3*0301 in Houston Caucasian patients when compared to Houston Caucasian controls (38 vs 11%, pc = 0.012, RR = 5.0).
Among the 15 HLA-DRB1, 3 DRB3, 9 DQA1, 15 DQB1, and 19 DPB1 alleles examined, none were found to be significantly associated with KS, except for an increased frequency of HLA-DRB3*0301 in Houston Caucasian patients when compared to Houston Caucasian controls (38 vs 11%, pc = 0.012, RR = 5.0).
Among the 15 HLA-DRB1, 3 DRB3, 9 DQA1, 15 DQB1, and 19 DPB1 alleles examined, none were found to be significantly associated with KS, except for an increased frequency of HLA-DRB3*0301 in Houston Caucasian patients when compared to Houston Caucasian controls (38 vs 11%, pc = 0.012, RR = 5.0).
Because mycobacterial HSP65, a cognate of human HSP63, is a common immunogen in bacterial species, and because the major immunopathologic feature of KD is reportedly an abnormally activated immune system, it suggests that an increased level of HSP63 gene transcription may be associated with the pathogenesis of KD.
A bacteriological study of isolates from the oral cavity of patients with Kawasaki disease (KD), age-matched non-KD patients and healthy children, showed that over half the KD and control isolates had gram-positive, catalase-negative cocci.
Patients with Kawasaki disease and coronary aneurysm more often than expected had the genotype II suggesting that reactions induced by the type of ACE polymorphism predispose to coronary aneurysm formation.
These results strongly suggest that B cells expressing kappa light chains with the 11 amino acid CDR3 domains might be involved in the pathogenesis of KD.
The plasma levels of interleukin (IL)-1beta, IL-2, IL-6, IL-8, IL-10, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and granulocyte colony-stimulating factor (G-CSF) were elevated in the acute phase of KD.
The plasma levels of interleukin (IL)-1beta, IL-2, IL-6, IL-8, IL-10, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and granulocyte colony-stimulating factor (G-CSF) were elevated in the acute phase of KD.
In contrast, serum levels of Hp between KD patients with Hp2-2 and with Hp1 allele (297 +/- 121 mg dL-1 vs. 330 +/- 101 mg dL-1, respectively) was not significantly different.
Duration of fever at diagnosis of KD was significantly different between patients with Hp 2-2 (6.4 +/- 1.2 days, n = 25) and with Hp1 allele (Hp 2-1 plus Hp 1-1; 8.8 +/- 3.5 days, n = 22).
To characterize both phenotypic (clinical features and magnetic resonance imaging [MRI] findings) and genotypic aspects of autosomal-dominant recurrent fever, also known as tumor necrosis factor receptor (TNFR)-associated periodic syndrome (TRAPS), in a French family and to investigate the role of the mutated 55-kdtumor necrosis factor alpha (TNFalpha) receptor (TNFR1) in the pathogenesis of the disease.
To characterize both phenotypic (clinical features and magnetic resonance imaging [MRI] findings) and genotypic aspects of autosomal-dominant recurrent fever, also known as tumor necrosis factor receptor (TNFR)-associated periodic syndrome (TRAPS), in a French family and to investigate the role of the mutated 55-kd tumor necrosis factor alpha (TNFalpha) receptor (TNFR1) in the pathogenesis of the disease.