Increased frequency of HLA-DR11 in pediatric human immunodeficiency virus-associated parotid gland enlargement.

We sought to determine whether an increased frequency of the HLA-DR11 (formerly DR5) phenotype is found in human immunodeficiency virus (HIV)-infected children with parotid gland enlargement. In HIV-infected adults, parotid gland enlargement may be part of the diffuse infiltrative CD8 lymphocytosis syndrome. An increased frequency of expression of HLA-DR11 has been described in association with diffuse infiltrative CD8 lymphocytosis syndrome. We conducted a case-control study with 26 HIV-infected children, 13 of whom had parotid gland enlargement and 13 of whom did not but who were matched for age, race, and sex with those with parotid gland enlargement. Clinical and laboratory parameters (including HLA-DR11 phenotype) were compared between the two groups. HIV-positive children with parotid gland enlargement showed an increased frequency of HLA-DR11, similar to their adult counterparts with diffuse infiltrative CD8 lymphocytosis syndrome. The HLA-DR11 phenotype may be associated with the development of parotid gland enlargement in HIV-infected children and may be a marker for a more benign outcome of HIV infection.

Enriched HLA-DQ3 phenotype and decreased class I major histocompatibility complex antigen expression in recurrent respiratory papillomatosis.

Respiratory papillomas, caused by human papillomaviruses, are benign tumors that recur following removal. We evaluated immune function and major histocompatibility complex (MHC) phenotype and expression in these patients. MHC-independent immune function appeared normal. The frequency of peripheral blood MHC class II phenotypes was highly enriched for DQ3 and DR11, one split of DR5. Class I MHC antigen expression on papilloma tissue was markedly reduced. Together, these phenomena may facilitate papillomavirus evasion of the cellular immune response.

Expression of the rheumatoid factor cross-reactive idiotype in JRA: association with disease onset subtype, disease activity and disease severity.

We previously reported that approximately one-third of patients with juvenile rheumatoid arthritis (JRA) express high concentrations of antibodies marked by the rheumatoid factor cross reactive idiotype (RCRI) in their sera (6). In order to determine if an expression of RCRI is associated with certain clinical features of the disease, we prospectively studied 49 patients with JRA over a six month period, and determined serum RCRI concentrations by inhibition ELISA. RCRI concentrations correlated significantly with the duration of morning stiffness (r = .3866, p less than .01), and the functional class (p less than .001), but not with the number of active joints. Expression of RCRI was higher in patients with systemic onset disease (p less than .03), compared to patients with pauciarticular or polyarticular disease. In patients studied on more than one occasion, the RCRI expression was relatively constant despite changes in disease activity. A subset of JRA patients with systemic onset disease, higher serum concentrations of the RCRI.

Identification of anti-idiotypic antibodies in the sera of ryegrass-allergic and nonallergic individuals.

Anti-idiotypic (Id) antibodies (Abs) are generated in the humoral response to antigen (Ag). Some of these anti-Id Abs are capable of binding to the combining site or paratope of Abs that bind Ag. These Ab2 can competitively inhibit the binding of Ab1 to Ag may trigger an Ab1 response similar to the response induced by Ag. To determine if specific Ab2 that inhibit the binding of IgE Abs to ryegrass (RG)-pollen allergens are present in the sera of RG-allergic (RGA) individuals before the initiation of allergen-specific hyposensitization with RG-pollen extract, we studied sera from five RGA and four nonallergic (NA) subjects in an IgE anti-RG RAST-inhibition assay. Ab2-enriched serum fractions were prepared from these study subjects by exhaustive mixed grass-pollen affinity chromatography to remove IgE and IgG anti-RG Ab1 from whole serum aliquots containing Ab1. Unabsorbed, twice-concentrated sera were diluted to one-time concentrated sera with equal volumes of either Ab2-enriched sera without Ab1 or borate-buffered saline absorbed by mixed grass-pollen affinity chromatography. IgE anti-RG Ab1 was determined by a standard RG RAST assay. We have detected Ab2 in the sera of the RGA patients, which inhibit the binding of autologous and allogeneic IgE anti-RG to RG Ags in solid phase. Parallel RG RAST assays with sera from NA subjects demonstrated no significant inhibition. Ab2-enriched sera from some grass-allergic and some NA subjects inhibited IgE anti-RG binding found in some RGA patients' sera. We conclude that anti-Id Abs, Ab2, specific for IgE anti-RG, Ab1, are present in some RGA patients and NA individuals.