References

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Charlton, B., and K. J. Lafferty. 1995. The TH1/TH2 balance in autoimmunity. Curr. Opin. Immunol. 7:793.

Erikson, J., et al. 1998. Self-reactive B cells in nonautoimmune and autoimmune mice. Immunol. Res. 17:49.

Hausmann, S., and K. W. Wucherpfennig. 1997. Activation of autoreactive T cells by peptides from human pathogens. Curr. Opin. Immunol. 9:831.

Horwitz, M. S., et al. 1998. Diabetes induced by Coxsackie virus: initiation by bystander damage and not molecular mimicry. Nature Med. 4:781.

King, C., and N. Sarvetnick. 1997. Organ specific autoimmunity. Curr. Opin. Immunol. 9:863.

Levin, M. C., et al. 2002. Autoimmunity due to molecular mimicry as a cause of neurological disease. Nat Med. 8:509.

Liblau, R. S., S. M. Singer, and H. O. McDevitt. 1995. TH1 and Th2 CD4+ T cells in the pathogenesis of organ-specific autoimmune diseases. Immunol. Today 16:34.

Lockshin, M. D. 1998. Why women? J. Am. Med. Womens Assoc. 53:4.

O'Garra, A., L. Steinman, and K. Gijbels. 1997. CD4+ T-cell subsets in autoimmunity. Curr. Opin. Immunol. 9:872.

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Silverstein, A. M., and N. R. Rose. 1997. On the mystique of the immunological self. Immunol. Rev. 159:197.

Steinman, L., J. R. Oskenberg, and C. C. A. Bernard. 1992. Association of susceptibility to multiple sclerosis with TCR genes. Immunol. Today 13:49.

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USEFUL WEB SITES

http://www.lupus.org/index.html

The site for the Lupus Foundation of America contains valuable information for patients and family members as well as current information about research in this area.

http://www.nih.gov/niams/

Home page for the National Institute for Arthritis and Mus-culoskeletal and Skin Diseases. This site contains links to other arthritis sites.

http://www.niddk.nih.gov/

Home page for the National Institute for Diabetes and Digestive and Kidney Diseases. This site contains an exhaustive list of links to other diabetes health-related sites.

http://www.sciencemag.org/feature/data/983519.shl

Link to a Web site that provides specific information concerning the role of gender in autoimmune disease.

Study Questions

Clinical Focus Question What are some of the possible reasons why females are more susceptible to autoimmune diseases than males?

1. For each of the following autoimmune diseases (a-m), select the most appropriate characteristic (1-13) listed below.

Diseases a. _Experimental autoimmune encephalitis

b. _Goodpasture's syndrome c. _Graves' disease d. _Systemic lupus erythematosus (SLE)

d. _Insulin-dependent diabetes mellitus

Go to www.whfreeman.com/immunology ^ Self-Test Review and quiz of key terms f. _Rheumatoid arthritis g. _Hashimoto's thyroiditis h. _Experimental autoimmune myasthenia gravis (EAMG)

i. _Myasthenia gravis j. _Pernicious anemia k. _Multiple sclerosis l. Autoimmune hemolytic anemia

Characteristics

(1) Auto-antibodies to intrinsic factor block vitamin B12 absorption

(2) Auto-antibodies to acetylcholine receptor

(3) TH1-cell reaction to thyroid antigens

(4) Auto-antibodies to RBC antigens

(5) T-cell response to myelin

(6) Induced by injection of myelin basic protein plus complete Freund's adjuvant

(7) Auto-antibody to IgG

(8) Auto-antibodies to basement membrane

(9) Auto-antibodies to DNA and DNA-associated protein

(10) Auto-antibodies to receptor for thyroid-stimulating hormone

(11) Induced by injection of acetylcholine receptors

(12) TH1-cell response to pancreatic beta cells

2. Experimental autoimmune encephalitis (EAE) has proved to be a useful animal model of autoimmune disorders.

a. Describe how this animal model is made.

b. What is unusual about the animals that recover from EAE?

c. How has this animal model indicated a role for T cells in the development of autoimmunity?

3. Molecular mimicry Is one mechanism proposed to account for the development of autoimmunity. How has induction of EAE with myelin basic protein contributed to the understanding of molecular mimicry in autoimmune disease?

4. Describe at least three different mechanisms by which a localized viral infection might contribute to the development of an organ-specific autoimmune disease.

5. Transgenic mice expressing the IFN-7 transgene linked to the insulin promoter developed diabetes.

a. Why was the insulin promoter used?

b. What is the evidence that the diabetes in these mice is due to autoimmune damage?

c. What is unusual about MHC expression in this system?

d. How might this system mimic events that might be caused by a localized viral infection in the pancreas?

6. Monoclonal antibodies have been administered for therapy in various autoimmune animal models. Which monoclonal antibodies have been used and what is the rationale for these approaches?

7. Indicate whether each of the following statements is true or false. If you think a statement is false, explain why.

a. Th1 cells have been associated with development of autoimmunity.

b. Immunization of mice with IL-12 prevents induction of EAE by injection of myelin basic protein plus adjuvant.

c. The presence of the HLA B27 allele is diagnostic for ankylosing spondylitis, an autoimmune disease affecting the vertebrae.

d. Individuals with pernicious anemia produce antibodies to intrinsic factor.

e. A defect in the gene encoding Fas can reduce programmed cell death by apoptosis.

Transplantation Immunology

B27 Positivo Autoinmune

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