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Gender Differences in Immune Response

This article explores the gender differences in immune response, focusing on how females may have a better ability to resist infections but also a higher risk of autoimmune diseases. It discusses the evidence supporting the role of hormones in human and murine lupus and the diagnostic challenges of lupus. Additionally, it covers the natural history of systemic lupus erythematosus (SLE), disease mimickers, and current standard and novel therapies.

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Gender Differences in Immune Response

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  1. Gender Differences in Immune Response Females resist a variety of infections better than males ??? Females may reject transplanted organs more rapidly Females have a higher frequency of autoimmune diseases

  2. Evidence to Support Hormone Role in Human Lupus • Female predominance • Disease  during pregnancy, menses •  Levels of androgen in women with lupus •  Frequency of lupus in Klinefelter (XXY) men •  Disease with estrogen administration ?

  3. Evidence to Support Hormone Role in Murine Lupus Mouse model lupus (NZB x NZW) disease identical to human F > M Female mice die earlier than males Male castration and estrogen accelerates disease Male sex hormones delay onset of lupus in female mice

  4. Role of Hormones on Immune Function Male hormones (androgen) suppress Female hormones (estrogen) enhance

  5. CRITERIA FOR THE DIAGNOSIS OF SLE (As revised in 1997 by the American College of Rheumatology) • A person is said to have SLE if four of these criteria are present at any time: • Skin criteria • Butterfly rash (lupus rash over the cheeks and nose) • Discoid rash (thick rash that scars, usually on sun-exposed areas • Sun sensitivity • Oral ulcerations • Systemic criteria • Arthritis • Serositis • Proteinuria or cellular urinary casts • Seizures or psychosis with no other explanation

  6. Diagnostic Challenges Con 1. Interpretation of criteria 2. Manifestations not in criteria 3. Other diseases may mimick lupus 4. Evolving symptoms over time 5. Patients may present very differently

  7. Disease Mimickers • Sjogren’s syndrome • Fibromyalgia (+ ANA) • Early rheumatoid arthritis • ITP • Primary antiphospholipid syndrome • Drug-induced lupus

  8. Natural History of SLE • Disease flares/activity (reversible) • Organ damage (irreversible) disease treatment

  9. SLE Damage SLE Activity 1 2 3 4 5 6 7 8 Time (years)

  10. Activity Nephritis Inflammation and medications Damage Renal failure/scar Osteoporosis/Fx Ovarian failure Myocardial infarction SLE Activity vs Damage

  11. SSA (Ro) SSB (La) RNP dsDNA Autoantibody Determined Clinical Subsets of SLE phospholipids Ribosomal-P ANA (+)>95% patients ANA + > 90%, nonspecific

  12. CD40L-CD40 Interactions TCR T-cell B Cell CD3 CD40 CD40L (gp39) CD40: B-cells, endothelial cells, macrophages, Ag-presenting cells, renal parenchymal, tubular, etc cells CD40L: T-cells, platelets

  13. SSA/SSB (rash and neonatal lupus, • dry eyes and mouth) dsDNA (kidney disease) Autoantibody Determined Clinical Subsets of SLE RNP (Raynauds) Phospholipid (clotting and miscarriage) Ribosomal-P (CNS, psychosis)

  14. Pathogenesis of SLE

  15. Current Standard Therapy Mild to Moderate DiseaseTherapy arthritis photoprotection fever NSAID pleurisy corticosteroids pericarditis methotrexate cutaneous antimalarials topical agents physical therapy

  16. Current Standard Therapy Moderate to Severe DiseaseTherapy nephritis corticosteroids vasculitis cyclophosphamide pneumonitis azathioprine CNS cyclosporine hematologic IVIg plasmapheresis ??? mycophenylate mofetil

  17. Novel Therapies Immunosuppressants T cells B cells Complement Cytokine Hormonal Immunoablation

  18. Lupus Center of Excellence 2004 Lupus Center of Excellence 2003

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