Search PubMed⌕ Search

PubMed · 8254182

Abnormal immune function in malignant hypertension.

Abstract

OBJECTIVE: To investigate the extent to which the immune system is influenced in patients with previous malignant hypertension. DESIGN: Twenty-three patients with malignant hypertension (fundus hypertonicus grades III or IV) in the Gothenburg area were studied over a 3-year period. After treatment had been instituted they were investigated to establish the function of the cellular immune system (number of T lymphocytes and the proliferative response to T-cell mitogens), human leucocyte antigens A, B and C and frequency of autoantibodies. METHODS: The numbers of T lymphocytes were quantified as erythrocyte rosettes. Lymphocyte-stimulation tests were carried out using the T-cell mitogens phytohaemagglutinin and concanavalin-A. Autoantibodies were determined with immunoassay techniques and leucocyte A, B and C antigens with a lymphocytotoxicity test. RESULTS: The frequency of T lymphocytes and their baseline thymidine incorporation were significantly depressed in patients with previously malignant hypertension compared with control subjects. The group with malignant hypertension also had a decreased proliferative response to concanavalin-A but not to phytohaemagglutinin, and they had an increased frequency of antinuclear antibodies. Human leucocyte antigen B15 tended to occur more frequently in patients with malignant and non-malignant hypertension than in control subjects, especially if a family history of hypertension was taken into consideration. CONCLUSION: The results from the present study indicate that immune mechanisms are involved in malignant hypertension, either secondary to the vascular damage or as a primary abnormality.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E Hilme, L Hansson, L Sandberg, T Söderström, H Herlitz. 1993. Abnormal immune function in malignant hypertension.. https://doi.org/10.1097/00004872-199309000-00014

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Analysis of HLA class I specific antibodies in patients with failed allografts.

BACKGROUND: The goals of this study are first to determine the epitope specificity of donor specific antibody (DSA) in the serum of alloimmunized transplant patients with a failed renal graft; and second to understand the correlation between the development of DSA and nondonor specific antibody (NDSA). METHODS: The sera of 35 pretransplant panel reactive antibody (PRA)-negative patients with failed allografts were examined with single-antigen (SA) luminex beads to identify human leukocyte antigen (HLA)-A and -B antibodies. Potential HLA antibody epitopes were identified by using computer software and verified by absorption and elution from single-antigen cell lines. RESULTS: Twenty-seven patients developed donor-specific HLA-A and/or -B antibodies, while the remaining eight patients had only nondonor-specific HLA-A and/or -B antibodies. The DSA-positive patients also had a long list of NDSA. Sixty-eight percent of the reactions found in 27 recipients with DSA were attributable to 66 epitopes on the mismatched donor HLA molecule. All 39 NDSA in eight patients with only NDSA shared 17 epitopes within positive allele specificities. By absorption and elution using recombinant cell lines having a single HLA specificity, we confirmed the epitopes involved in three patients. CONCLUSION: Development of most NDSA in patients with failed allografts is likely due to sharing epitopes with DSA and/or other NDSA.

Antibody Formation↗

Human keratinocyte Toll-like receptors promote distinct immune responses.

It has been well established that Toll-like receptors (TLRs) are expressed by keratinocytes and respond to their respective ligands to initiate immune responses. However, it appears that keratinocytes, via differential activation of TLRs, may play a key role in determining the type of subsequent cutaneous immune response generated against a particular pathogen.

Antibody Formation↗