Inflammation and the Immune Response

Major Portals of Antigen Entry into the Body

  1. Skin
  2. Respiratory tract
  3. Gastrointestinal tract

Possible Outcomes of Inflammatory Response

  1. Elimination of the causative agent
  2. “Walling off” of the inflammation from the rest of the body (delays the spread of bacteria or toxins) to allow for healing
  3. Persistence of the causative agent leading to chronic inflammation or spread throughout the body

Major Families of Adhesion Molecules

  • Selectins
  • Addressins
  • Integrins
  • Immunoglobulin superfamily

Activated Macrophages: Major Secretory Cells Able to Synthesize Over 100 Products Including Immunoinflammatory Mediators

Acute Phase Proteins: Plasma Proteins Whose Concentrations Change by at Least 25% During Inflammation

  • Made in the liver
  • Play role in the innate immune response to infectious agents

Acute Phase Response

  • Fever
  • Leukocytosis (hematopoiesis)
  • Increased synthesis of acute phase proteins in liver
  • Decrease in plasma concentration of iron
  • Decrease in appetite
  • Increased secretion of many hormones (ACTH and Cortisol)

Adaptive Immunity: Mediated by T and B Cells, This Is Highly Specific for a Pathogen. It Takes Several Days for the System to Become Fully Functional. The Response Improves with Each Encounter with the Same Pathogen (It Has a Memory for Pathogens). This Makes Up the Third Line of Defense for the Host.

  • Slow onset (days to weeks)
  • Antigen specific
  • Has memory to pathogens, so it will respond to Vaccs.
  • T and B lymphocytes

Addressin: Mucin-Like Family That Have Carbohydrate Regions That Bind to Selectins. Expressed on Surface of Leukocytes and Endothelial Cells.

  • GlyCAM-1, CD34, PSGL-1, ESL-1

Adherence of Neutrophils: Once a Neutrophil Encounters the Microbe, It Must Bind to It. This Is Mediated by the Interaction Between Cell Surface Receptors and Ligands on the Microbe.

Alpha (Heavy) Chain (44-47kD) MHC Class 1: There Are Three Domains, Alpha 1, 2, and 3 and a Transmembrane Cytoplasmic Tail. Binding Happens in the Peptide Binding Cleft for Peptides of 8-11 Amino Acids.

**Each can bind several different antigenic peptides but only one at a time.

Alternative Pathway: We Don’t Need IgG or IgM to Start This Pathway So We Can Use It the First Time We See an Antigen and Occurs on the Microbial Surface. Activated by Gram – and Gram + Bacteria.

  • Starts with C3 tickover from natural hydrolysis

Antagonism: A Cytokine May Antagonize the Effects of Another Cytokine

Antibody-Mediated (Humoral) Immunity: Component of the Specific Immunity. Antibodies That Are Produced Because of an Interaction Between an B Lymphocyte and an Antigen. Most Effective in Eliminating Extracellular Antigens and Bacterial Toxins

Antigens: Substances That Can Induce Humoral and/or Cell-Mediated Immune Responses When Introduced. The Antigen Must Be Able to React Specifically with the Antibodies or Sensitized T Cells Produced Against It.

Antiproteinases: Synthesized by the Liver, Leukocytes, and Connective Tissue – Inhibitleukocyte Proteinases Thereby Preventing and/or Minimizing Tissue Damage

B Cell Differentiation and Maturation (In Birds): Majority of B Cells (90-95%) Die Through Apoptoisis (Negative Selection of Self-Reactive B Cells. Mature B Cells Begin to Migrate from the Bursa to the Peripheral Lymphoid Organs a Few Days Before Hatching

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What will the compliment system kill? – Will only lyse gram – bacteria because they have a very thin peptidoglycan layer.