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Home , Immune disorder, Poison ivy

DON’T TOUCH THE POISON IVY!

Fantastic Voyage Revisited: a conversation about the , allergic , and selected immunological issues OUTLINE OF ACTIVITY

 An overview of the immune system and vaccination stories (45 min) followed by a 15 minute break.  Hypersensitivity (Bee stings and Poison Ivy), and stories (45 min) followed by a 15 minute break.  Selected immune disorders [, Type I , HIV/AIDS, & one Zoonotic Example] (45 min) followed by discussion 15 minutes.  *Constant questioning would be appreciated, let’s make this a conversation rather than a lecture! LET’S BEGIN THE FANTASTIC VOYAGE WHY DO WE NEED AN IMMUNE SYSTEM? BACTERIA, , FUNGI, PARASITES & NEOPLASTIC CELLS THINGS TO REMEMBER ON THE JOURNEY!

Recognition Specificity Regulation Memory SO WHAT MAKES UP AN IMMUNE SYSTEM WHOA! ANTIGEN PRESENTATION AND T-CELL HELP & MEMORY HUMMORAL IMMUNITY B-CELL ACTIVATION STRUCTURE KILLING OF MICROBES BY ANTIBODY CELLULAR IMMUNITY KILLING OF MICROBES BY CELLULAR IMMUNITY VACCINATION VACCINATION RATIONALE

 Vaccine Development  Observations of natural immunity  Identification of immunological targets  Formulation and manufacturing  Clinical trials, safety, efficacy  Marketing  Expected Outcome  Elimination of clinical infection  Eradication of disease  All in the presence of evolving organisms, politics, opinions, legal challenges, and markets HOLD THAT THOUGHT! WE WILL BEGIN TO IN THE NEXT HALF HOUR. IGE-DEPENDENT IMMUNE RESPONSES & ALLERGIC DISEASE ACTIVATION OF TH2 CELLS AND PRODUCTION OF IGE

 Nature of

WHAT HAPPENS UPON EXPOSURE TO (ANTIGEN) MAST CELLS, BASOPHILS, & EOSINOPHILS & BASOPHIL MEDIATORS

 Biogenic amines  Granule enzymes  Proteoglycans  Cytokines  Lipid mediators

 Prostaglandin D2  Leukotrienes

EOSINOPHIL MEDIATORS

 Granule proteins that are toxic to parasitic organisms and may injure normal tissue.  Major basic protein  Eosinophil cationic protein  Eosinophil peroxidase  Lipid mediators THE IMMEDIATE REACTION

 The wheal and flare reaction THE LATE-PHASE REACTION IGE MEDIATED ALLERGIC DISEASES

 Systemic Anaphylaxis ANAPHYLAXIS

 Vasodilation, fall in blood pressure (shock)  Smooth muscle constriction of upper and lower airways, laryngeal edema, hypermotility of the gut, outpouring of mucous in the gut and respiratory tract, in the skin (respiratory distress)  Epinephrine (adrenalin) reverses bronchoconstriction, vasodilation and increases cardiac output  Antihistamines may also be beneficial OTHER IGE MEDIATED ALLERGIC DISEASES

 Bronchial  Food  Urticaria and Eczema

IMMUNOTHERAPY

 Desensitization ( shots)  Shift from IgE to IgG

 Specific tolerance Th2 to Th1 SO WHAT IS THE VALUE OF IGE & MAST CELLS?

 Protection against parasites  Mast cells play an important protective role as part of innate to bacterial infections  Slower bleeding time in atopics, sudden cardiac arrest less common  As a result of heightened response, protection against arthropod vectored diseases (my speculation)  Just an unfortunate consequence of otherwise protective responses. The price we have to pay?  Or have some organisms through evolution co-opted hypersensitivity to there own benefit (toxins)? CUTANEOUS “DELAYED” T-CELL MEDIATED HYPERSENSITIVITY

 Poison Ivy/Poison Oak  Contact allergens  ALLERGIC DISEASE IN CATTLE: PSOROPTIC SCABIES (COWS ITCH TOO!!) YES!! ADDITIONAL IMMUNOLOGICAL TOPICS

, > 30 diseases or syndromes  Transplantation  Neuroimmunology  Reproductive immunology  Tumor immunology

AUTOIMMUNE HEPATITIS

 Infection of the liver with the hepatitis B (HBV, serum hepatitis)  350 million people affected worldwide  Little cytopathology caused by the virus  Liver damage can be massive and devastating  When serious damage occurs, it is the immune system that causes most, if not all, of the damage  Both CD4 and CD8 cells are activated and a delayed-hypersensitivity reaction ensues. AUTOIMMUNITY: DIABETES (TYPE I) INSULIN DEPENDENT

 Age of onset 11 to 12 years  Chronic autoimmune disease destroying the insulin + producing βcells in the pancreas (CD4 TH1, Cytokine TNF and IL-1, and potentially anti-insulin )  No gender bias  Strong genetic component (HLA-DR3, DR4)  Possible onset with environmental “triggers”  Viral infection, an example Serotype B Coxsackie virus  Tandem repeats within the insulin promoter (genetic)  T cells the major destructive agent with antigen being glutamic acid decarboxylase (GAD). Insulin itself also appears to be a target.  Epidemiology data suggest that repeated infection protects from diabetes. Possible reason for increase incidence in developed countries.  New Therapies: inducing immunological tolerance, generating or giving regulatory T cells to patients.

A AFFECTING THE IMMUNE SYSTEM: HIV/AIDS

 First reported in 1981, opportunistic infections, Pneumocystis carinii, oral candidiasis, tuberculosis, and Kaposi’s sarcoma  The human virus (HIV) was identified in 1983 as a retrovirus.  The coat proteins mutate at an extraordinarily high rate.  Infects and causes a gradual loss of CD4 helper T cells  Drug treatment is of 4 categories: nucleoside analogs, reverse transcriptase inhibitors, protease inhibitors and fusion inhibitors. HIV

 HIV has a surface coat protein gp 120 that specifically recognizes and binds to the CD4 molecule found on CD4 T cells  Following binding the gp 120 molecule twists and reveals a second binding molecule gp 41 that binds a second coreceptor of the CD4 cell surface, called fusin. With both binding events the virus can enter the cell.  Therapy  Drug Cocktails – enfuvirtide blocks gp 41/fusin  Vaccine is available for SIV and FIV, and observe cases of natural effective immunity. DNA based vaccine/CD8 preferential stimulation  Molecular Medicine (gene therapy) antisense with target of suppression of fusin  Selective expression of thymidine kinase and treatment with acyclovir ZOONOTIC IMMUNE DISORDER: CATTLE GRUB, HYPODERMA LINEATUM IMMUNE DISORDERS

 Human Case of Cattle Grub Infestation

THE END BUT STAY TUNED