exam 4

• Immunodeficiency


  Immune components do not work
• Phylaxis


  Protection against infection
• Anaphylaxis


  An immediate hypersensitivity reaction triggered by cell degranulation. It can be local or systemic.
• Prophylaxis


  Measures designed to preserve health and prevent the spread of disease; protective or preventative treatment.
• Types of hypersensitivity


  • Immediate
  • Delayed (DTH)
• IgE-mediated hypersensitivity


  1. Exposure to allergen activates t-helper cells

  2. Stimulation of B-cells to form IgE-secreting plasma cells

  3. IgE binds to IgE-specific Fc receptors on mast cells and basophils (now sensitive for next exposure)

  4. Second exposure to allergen= cross-linking if IgE (triggers degranulation)
• Cytoplasmic granule effects


  • Vasodilation
  • Vascular permeability
• Common allergens associated with type I hypersensitivity

  • Allergens: antigens that induce type I hypersensitivity
• Manifestations of type I hypersensitivity

  • Systemic anaphylaxis
  • Local anaphylaxis (more common): Allergic rhinitis, Asthma, Food allergies, Atopic dermatitis
• Effects of degranulation


  • Anaphylactic shock: often fatal within minutes (skin or gut)
  • Bronchial constriction: asphyxiation
• Describe the naturally occurring CRISPR system found in bacteria and Archaea. How does this mechanism function as an immune response?


  CRISPR

  • Creates strands of viral RNA with a barcode

  1. CAS recognizes viral DNA
  2. Pieces get incorporated into host genome
  3. Generates memory component of virus
  4. Transcription of viral DNA+ barcode

  • Guided RNA targets virus for destruction

  AMP- antimicrobial peptides
• Explain the role of AMP in the immune response, particularly in systems other than vertebrates.

  Intracellular killing mechanisms

  1. inhibits cell wall synthesis
  2. Alters cytoplasmic membrane
  3. activation of autolysin
  4. Binds to DNA
  5. Inhibits DNA, RNA, and protein synthesis
  6. inhibits enzymatic activity
• What broad functional categories do AMP fall under?

  Cell surface targeting and intracellular targeting
• Describe the two main categories found as part of a plant immune response.

  PAMP triggered immunity: PAMP, MAMP, DAMP, HAMPS, PRR recognition

  Effector mediated immunity: ROS, NOS, AMP, Lysosomes
• Drosophila


  Fruit fly
• Drosophila immune responses


  • AMB's
  • Prophenoloxidase cascade- forms nodule
  • Hemocytes – WBC
• Hemocytes


  • Initiate wound repair
  • Blood coagulation
  • Phagocytosis
  • Nodules
  • Encapsulation
• RNA silencing/interference


  1. Pre-miRNA -> cytoplasm -> cleaved into mature miRNA by DICER->enzyme cleaves dsRNA into small pieces

  2. Mature miRNA binds to RISC (RNA-induced silencing complex) -> contains proteins including ribonuclease

  3. MiRNA binds to matching sequence of mRNA

  4. MiRNA+ RISC + mRNA = cleaves mRNA = inhibition of a gene into a protein
• Hypersensitivity


  Immune response that is exaggerated or inappropriate
• Types of Hypersensitivity


  • Type I- IgE-mediated
  • Type II- Antibody-mediated cytotoxic
  • Type III- Immune complex-mediated
  • Type IV- Delayed type (DTH)
• Type I- IgE-mediated Hypersensitivity

  1. Cross-linking of IgE to mast cells

  2. Release of histamine and heparin from mast cells or basophils
• Type II- Antibody-mediated cytotoxic


  • Antibodies mediate destruction via complement of ADCC
  • Antibodies activate the classical pathway-> MAC
  • Leads to acute inflammation
  • Antibodies can bind to self-antigen
  • Can lead to infant death in RH- mothers
• Type III- Immune complex-mediated

  • Too much lytic activity
  • AB complexes not cleared
  • Inflammation/cell recruitment persists
  • Same type of ID as rheumatoid arthritis (response to self) or response to penicillin (drug allergies)
• Type IV- Delayed type (DTH)


  1. Only hypersensitivity without antibodies

  2. Takes 2-3 days to develop

  3. Requires subsequent re-exposure to antigen

  4. Antigen binds to TH cell MHC II

  5. TH cell releases cytokines

  6. Influx of phagocytic cells to site

  7. Cytotoxic T cell activation

  8. Defined by an excess of cytokines in response to component
• Type IV- Delayed type (DTH)


  • Poison ivy and poison oak
• Hypersensitivity


  Exaggerated response to self or foreign antigen
• Autoimmunity


  Improper response of immune system against self-antigen
• Tolerance


  Mechanisms that exist to protect an individual from potentially harmful self-antigen attacking t-lymphocytes
• Central tolerance (main mechanism)

  Deletion of overactive lymphocytes in thymus
• Peripheral tolerance (extra safety net)

  If a lymphocyte is overactive to self-antigen, it either undergoes apoptosis or anergy
• Factors that promote tolerance

  • High-doses of antigen
  • Persistence of antigen in host
  • IV or Oral introduction
  • Absence of adjuvants
  • Low levels of costimulators
• Treg cells


  Cells that are reactive to self-antigen and have the ability to interact with T cells that are highly reactive to self-antigens and suppress the immune response
• Foxp3


  Transcription factor responsible for the development of T thymocytes into Treg cells with intermediate affinity for self-antigen
• 1. 8% of the population has an autoimmune disorder, 80% of these are female
• This is in part due to hormonal differences, where females have a stronger immune response
• Organ specific autoimmunity


  Autoimmune response has a specific target antigen, limited to a specific organ
• Systemic autoimmunity


  The autoimmune response targets an antigen that has a broad range (the antigen is not specific to one organ)
• APECED


  A systemic autoimmune disease caused by a single gene mutation, which codes for AIRE (component that develops every single self-antigen for thymocyte regulation)
• IPEX


  Mutation in Fox3p gene, fatal
• Graves disease


  Organ specific autoimmune disease involving the thyroid and TSH