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Literature DB >> 646466

Immune response inversion after hyperimmunisation. Possible mechanism in the pathogenesis of HLA-linked diseases.

Abstract

The crosstolerance hypothesis suggests that animals sharing antigens with some microorganisms will produce low antibody levels in the early part and high levels in the latter part of an infection. Antibody responses have been measured in high responder B10.M and B10.D2 mice and low responder C3H and A.Thy-1.1, as well as F1 hybrids (B10.M X A.Thy-1.1) and (B10.M X C3H/He), after repeated immunisation with the antigen ferritin, involving altogether 483 mice. An inversion in the immune response was found to occur and similar delayed high antibody responses have been described in rheumatic fever. It is suggested a mechanism of immune inversion may operate in the pathogenesis of HLA and blood group-linked diseases.

Entities: Disease Gene Species

Mesh：

Substances：

Year: 1978 PMID： 646466 PMCID： PMC1001181 DOI： 10.1136/ard.37.2.152

Source DB: PubMed Journal: Ann Rheum Dis ISSN： 0003-4967 Impact factor: 19.103

22 in total

1. Genetic control of the immune response in rats to the known sequential polypeptide (Tyr-Glu-Ala-Gly)n. I. Antibody responses.

Authors: A A Luderer; P H Maurer; R T Woodland
Journal: J Immunol Date: 1976-10 Impact factor: 5.422

6. Frequency of faecal Klebsiella aerogenes in patients with ankylosing spondylitis and controls with respect to individual features of the disease.

Authors: C J Eastmond; H E Willshaw; S E Burgess; R Shinebaum; E M Cooke; V Wright
Journal: Ann Rheum Dis Date: 1980-04 Impact factor: 19.103

6 in total

Immune response inversion after hyperimmunisation. Possible mechanism in the pathogenesis of HLA-linked diseases.

1. Genetic control of the immune response in rats to the known sequential polypeptide (Tyr-Glu-Ala-Gly)n. I. Antibody responses.

Review 2. DEPENDENCE OF ANTIBODY RESPONSES ON STRUCTURE AND POLYMORPHISM OF AUTOLOGOUS MACROMOLECULES.

3. Codominant inheritance in immunogenetic (IR-gene) systems.

4. Genetic control of the immune response to ferritin in mice.

5. Cross-reactivity in the radioimmunoassay of ferritin with cells from high- and low-responder mice.

6. HL-A, immune-response genes, and disease.

7. Gross reactivity between synthetic T,GA-L and transplantation antigens in CBA Mice.

8. Genetic control of the immune response to ferritin in F1 hybrid mice.

9. Ankylosing spondylitis: klebsiella and HL-A B27.

10. Association of H-2 types with genetic control of immune reponsiveness to IgG (gamma2a) allotypes in the mouse.

1. A reinvestigation of the cross-reactivity between Klebsiella and HLA-B27 in the aetiology of ankylosing spondylitis.

2. Identification of HLA-B27M1 and -M2 cross-reactive antigens in Klebsiella, Shigella and Yersinia.

3. Sequential studies in ankylosing spondylitis. Association of Klebsiella pneumoniae with active disease.

4. C-reactive protein, ESR, and klebsiella in ankylosing spondylitis.

5. Ankylosing spondylitis, HLA-B27 and Klebsiella. I. Cross-reactivity studies with rabbit antisera.

6. Frequency of faecal Klebsiella aerogenes in patients with ankylosing spondylitis and controls with respect to individual features of the disease.