Intro to immunology Flashcards
Normal immune system is made up of these 3 things….
Physical barriers
Innate immunity
Adaptive immunity
Physical barriers
Saliva - lysozyme - IgA - IgG - lactoferrin Mucociliary escalator Gastric acid Normal flora Physical flushing - urinary tract
Examples of consequences of breached defences
Xerostomia
C diff infection
Cystic fibrosis
Burns
Features of innate immunity
Rapid
Already present at birth
No memory - same response with re-exposure
Some specificity
What does innate immunity detect?
Alteration from homeostasis
- damage recognition - host
- pathogen recognition - pathogen
Where is the innate immunity found?
Within tissues
Within blood
Cells of the innate immunity
NK cells basophils Neutrophils eosinophils Monocytes Platelets Macrophages Dendritic cells Mast cells
Mechanisms of innate immunity
Inflammation Recruitment of immune cells Activation of complement Opsonisation Phagocytosis NK cytotoxicity
What do cytokines do?
Regulate the nature, duration and intensity of the immune response
Form a method of communication between components of the immune system
Bind to specific receptors on target cells
What predominately produces cytokines?
Macrophages
T helper cells
Two types of cytokines
Pro-inflammatory - TNF-a - IL-1 - IL-6 - Chemokines Anti-inflammatory - IL-10 - TGF-B
Pro-inflammatory cytokines cause…..
Fever
Recruit and activate other immune cells
vasodilation
What does IFN-y activate?
Macrophages
What does IL-3, IL-4, IL-5 and IL-13 activate?
Eosinophils
Mast cells
What does IL-4, IL-5, IL-6 and IL-21 activate?
B cells
What does IL-2, IL4, IL-12 and IFN-y activate?
T cells
What causes inflammation of the innate immune system?
Detection of ‘foreign’ / breach in defences by pattern recognition receptors (PRRs)
Features of inflammation and what causes each
Vasodilation - NO - Bradykinin - prostaglandins - TNF-a, IL-1 Increased vascular permeability - histamine - nitric oxide - leukotrienes Increased cell adhesion molecules - TNF-a, IL-1 Chemotaxis - CXCL-8 - neutrophil recruitment into the area Increased sensitivity to pain - bradykinin
Activation of complement
Activation of C3
- activated by
- alternative (pathogens)
- classical (combination of own antibodies bound to foreign antigens)
- lectin (free floating proteins in body attaching to pathogens)
Splits into C3a and C3b
- C3b splints into C5a and C5b
- C3a and C5a - anti-inflammatory toxins or protein which will affect mast cells to degranulate
C3a = inflammation C5a = chemotaxis
What is C5b?
Membrane attack complex
Activity of complement
- Chemotaxis of phagocytes to sites of inflammation
- C3a, C5a - Opsonisation
- C3b, C4b
- preparation for eating (reduces repellent negative cell charge and increases no of binding sites for phagocytes) - Lysis of micro organisms
- C5b-9 complex - Maintain solubility of Ag / Ab complexes
- C3b, C4b, C2
Main opsonins
Complement C3b, C4b
Antibodies
Plasma proteins - mannose binding lectin
Phagocytosis is done against what?
Extracellular pathogens
Two receptors on NK cytotoxicity
Activation
- if foreign pathogen / damaged cell
Inhibitory
- if normal cell
Features of the adaptive immune system
Specific Delayed Immunological memory - faster responses to known antigen Humoral - antibody mediated - B lymphocytes Cell mediated - T lymphocytes
Two types of cells in the adaptive immune system
B cells (can lead to plasma cell) T cells
Where do B cells mature?
Bone marrow
Where do T cells mature?
Thymus
Where do B and T cells migrate to once matured?
Secondary lymphoid organs where they encounter antigens