A higher frequency of HLA-A*02-allele in AS<sup>+</sup> patients compared to AS<sup>-</sup> controls (<i>p</i> = .015) and an accumulation of HLA-A*02-allele in AS<sup>+</sup> anti-VZV<sup>+</sup> group (33.3%, <i>p</i> = .004) was observed.
A higher frequency of HLA-A*02-allele in AS<sup>+</sup> patients compared to AS<sup>-</sup> controls (<i>p</i> = .015) and an accumulation of HLA-A*02-allele in AS<sup>+</sup> anti-VZV<sup>+</sup> group (33.3%, <i>p</i> = .004) was observed.
Allergic drug reactions are unpredictable; nevertheless, there is increased risk of drug hypersensitivity in (1) patients with cystic fibrosis who receive antibiotics; (2) patients with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) who receive trimethoprim-sulfamethoxazole or if human leukocyte antigen (HLA)-B*5701+ and receive the antiretroviral agent abacavir; (3) other genetically susceptible populations, e.g., Han-Chinese with HLA-B*1502+ who develop Stevens-Johnson syndrome and toxic epidermal necrolysis from carbamazepine, with HLA-B*5801+ who are at increased risk for such reactions from allopurinol, those with HLA-A*32:01 and receive vancomycin and develop drug reaction with eosinophilia and systemic symptoms syndrome; and (4) patients with a history of compatible allergic reactions to the same medication, similar class, or potentially unrelated medication.
HLA-A*02:07 was also identified as a possible risk allele for hypertension (OR 2.90; p < 0.05), and C*01:02 was a possible risk allele for dyslipidemia (OR 3.36; p < 0.05), both known to be common comorbidities in patients with psoriasis.
Statistical tests uncovered three protective alleles: HLA-A*11:01, associated with all forms of male infertility (p = 0.0006); HLA-DQB1*03:02 with SHV and OLI (P<sub>SHV</sub><sub> </sub> = 0.0303, P<sub>OLI</sub><sub> </sub> = 0.0153); and HLA-A*29:02 with OLI (p = 0.0355), which was found to interfere in sperm number together with HPV (p = 0.0313).
The discovery of an HLA-A*29:02/HPV crosstalk, together with former reports of HLA alleles conferring resistance-susceptibility to diverse human pathogens, raises the hypothesis of a mechanistic link between male infertility, HLA polymorphism, and host response to STD.
We aimed to study (1) to what extent the influence of low sun exposure on multiple sclerosis (MS) risk is mediated by low vitamin D levels; (2) whether low sun exposure or vitamin D deficiency act synergistically with HLA-DRB1*15:01 and absence of HLA-A*02:01.
MHC class I HLA-A association was sex related to both the total white adult type 3 PGA collective (n = 158, P = 0.0065), as well as in PGA patients with autoimmune Hashimoto thyroiditis (n = 91, P = 0.010).
We performed multivariable regressions on age at diagnosis, infection duration, and age at infection onset using these variables, as appropriate: sex; age at diagnosis; diabetes; autoimmune condition(s); atopy; allergy; corticosteroid use; body mass index; serum immunoglobulin isotype levels; blood lymphocyte subsets; three IgGSD-associated human leukocyte antigen-A and -B haplotypes; and referring physician specialties.
HLA-A*02:07 was also identified as a possible risk allele for hypertension (OR 2.90; p < 0.05), and C*01:02 was a possible risk allele for dyslipidemia (OR 3.36; p < 0.05), both known to be common comorbidities in patients with psoriasis.
These TCRs mediated recognition of commercially available ovarian cancer, uterine carcinoma, and myeloma cell lines, as well as an NIH patient-derived esophageal adenocarcinoma line that endogenously expressed p53 p.R175H and HLA-A*0201.
We also observed an association between nail psoriasis and HLA-A*02:07 carriers (OR 4.50; p = 0.002), whereas C*06:02 carriers were less prone to have nail involvement (OR 0.16; p = 0.004).
DYSF is upregulated and exhibits a potential role along with that of HLA-A and MCP-1 in inflammatory cell infiltration and muscle damage during the development of DM/PM.
TRB-J1 usage, in combination with the HLA-A*01:01 allele, represents an apparent survival advantage for uterine corpus endometrial carcinoma: Comparisons with microscopic assessments of lymphocyte infiltrates.
(5) The frequency of HLA-A*30:01 allele in complete response + partial response group was higher than stable disease + progressive disease group (P ≤ 0.05).
(5) The frequency of HLA-A*30:01 allele in complete response + partial response group was higher than stable disease + progressive disease group (P ≤ 0.05).
Our results identify a difference between HLA A*26 in patients who develop BIA-ALCL and the general population, and may signify genetic susceptibility factors responsible for germline genetic variation in HLA in patients with BIA-ALCL.
Gene-modified autologous T cells expressing NY-ESO-1<sup>c259</sup>, an affinity-enhanced T-cell receptor (TCR) reactive against the NY-ESO-1-specific HLA-A*02-restricted peptide SLLMWITQC (NY-ESO-1 SPEAR T-cells; GSK 794), have demonstrated clinical activity in patients with advanced synovial sarcoma (SS).
We previously reported that an association of maternal microchimerism (MMc) in BA and a significant compatibility of HLA-A between the patient with BA and their mother.
We designed conditional peptides for HLA-A*02:01 and H-2K<sup>b</sup> that form stable peptide-MHC I complexes at low temperatures, but dissociate when exposed to a defined elevated temperature.