Immue System - How are cells recruited to the site of infection?

Immue System - How are cells recruited to the site of infection?

1. Innate I.S. Recruitment

   • Involve...
     • Selectin + Chemokines + serpentin receptor adhesion
       • chemokine: I(V)CAM-1
       • Mechanisms
         • 1) Rolling adhesion
           • Following infection mast cells release vasodilators
             • ie. IL-1 and TNF-alpha
               • (i) they bind to their receptors activating endothelial cells
             • enable vascular endothelial cells to increase their expression of (produce) adhesion molecules
               • adhesion molecules
                 • Selectin
                   • cause leukocytes to slow their flow and roll along the inner blood vessel wall
                 • Chemokines
                   • Intracellular adhesion molecules (ICAM)
                   • Vascular cell adhesion molecule (VCAM)
               • Hence, increases capillary permeability
                 • allowing plasma + leukocytes (white blood cell) to leave bloodstream and enter tissue
         • 2) Tight binding
           • Chemokines (IL-8) at the inner suface of endothelial cells
             • interact with the chemokine receptors on the surface of rolling leukocytes
               • This triggers activation of intergrin on the surface of leukocytes
                 • This enables rolling leukocytes bind to VCAMs and ICAMs on the inner surface of vascular endothelial cells
         • 3) Diapedesis + Migration
           • Following the binding, diapedesis take place; leukocytes cross through the intact walls of the vascular endothelial cells and basement membrane
           • And migrate to the infection site
     • Mast cell
       • 1) Damaged mast cell releases histamine
       • 2) Histamine diffuses into capillaries
       • 3) Histamine causes capillaries to dilate and leaky, while complement proteins attract phagocytes
       • 4) Plasma and phagocytes move from capillary to the infection site
       • 5) Phagocytes engulf bacteria + dead cells
       • 6) The signalling of histamine and complement stop
         • phagocytes are no longer moving to the infection site
           • The tissue returns
       • ie. IL-1 and TNF-alpha

2. Other recruitment

   • Plasma entering the tissue
     • Complement proteins
       • bacteria in plasma activates complement
         • causes
           • cell lysis
           • WBC chemotaxis
       • acts with Beta defensins
     • Antibodies
       • Opsonisation occur to bacteria in extracellular
         • then ingestion by macrophage
         • + cell lysis
       • Cell lysis
       • Neutralisation of virus / toxins
         • then ingestion by macrophages
       • Immoblisation of microbes
       • Agglutination of microbes
         • defn: binding antigens to its corresponding antibody
       • blocking microbial adhesion
     • Lysozyme
       • Breaks down peptidoglycan with metalloprotease
     • Platelets and clotting factors
       • i) Stoppage bleeding
       • ii) Localisation of infection
         • means restrict the spreading of infection
       • WBC chemotaxis
         • chemotaxis defn:
           • movement of WBC in response to chemical stimulus
     • Beta-defesins
       • Alter cytoplasmic membrane
     • Nutrients
       • Feed inflammed tissue
     • Transferring
       • Traps iron
   • Cells entering tissue
     • Basophils
       • release histamine
         • Further promote inflammation
     • Eosinophils
       • moderation of inflammatory response by low affinity IgE receptor
       • Release lytic mediators on parasitic surface and affects inflammatory process
     • Neutrophils
       • synthesis inflammation mediator
     • B lymphocytes
       • Differentiate into plasma cells
         • Produce antibodies
     • T lymphocytes
       • Release cytokines
     • Monocytes
       • Become macrophages
         • process antigens + release chemokines
           • IL1-beta
           • IL6
           • IL12
           • CXCL8
           • TNF-alpha