1 / 31

Immune Response to Infection

Immune Response to Infection. Infectious Agents. Viruses Bacteria Parasites Protozoa. Primary response:. Natural Killer Cells: Non-antigen specific. These cells attack any foreign microbe in the body and attempt to kill it. Macrophages :

calvin
Télécharger la présentation

Immune Response to Infection

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Immune Response to Infection

  2. Infectious Agents • Viruses • Bacteria • Parasites • Protozoa

  3. Primary response: • Natural Killer Cells: • Non-antigen specific. • These cells attack any foreign microbe in the body and attempt to kill it. • Macrophages: • Respond to all invading microbes, ingest and kill. • Presents antigens from the microbe cell wall on the external cell wall of the microphage to activate T cells.

  4. Secondary response: • B Cells respond to antigens by differentiating into plasma cell. • Plasma Cells: • Secrete one specific antibody for a particular antigen based on the cell line from the B cell. • Helper T Cells: • Secrete interleukin hormone to stimulate clonal growth of activated T and B cells.

  5. Tertiary response: • CytotoxicT Cells: • Bind to body cells infected by the microbes and secrete toxic substances killing cell and invader. • Antibodies: • Complex with antigen which aggregates microbes together to deactivate the organisms.

  6. Viral Infections

  7. Overall Response to Viral Infections

  8. Innate Immune Response

  9. T cell activation DCs can be directly infected by virus. If DCs are not infected by virus, DCs can still internalize viral antigens from the suroundings through phagocytosis, endocytosis and macropinocytosis. The antigens can be presented in the context of both class II and class I MHC through cross-priming. Lysis of infected cells DCs are activated by recognition of Viral PAMPs through TLRs. Secondary lymphoid tissues DC CTL CD8 T cell Ag-MHC I virus infection TH1 Ag-MHC II CD4 T cell IL12 IFN- Viral antigen Endocytosis Pinocytosis phagocytosis TH1 failitates CD8 T cell activation by producing IL2 and activation of DCs through CD40L-CD40

  10. B cell activation DC TH cells antibodies Viral antigen B cell activation B cell Natural antibody Seoncdary lymphoid tissues FDC Antigen-antibody complex B1 cells

  11. Antibody Interaction with Viruses • Neutralize • Advantage antibodies to be at site of entry – mucosal surface • SecretoryIgA in mucous secretions plays an important role in host defense against viruses by blocking viral attachment to mucosal epithelial cells

  12. Viral Response to Host Immune Response • HCV (Hepatitis C Virus) Evades Anti-viral Effect Of IFNs By Inhibiting Action Of PKR • HSV (Herpes Simplex Virus) Decreases Expression Of MHC I, Avoids CTL Elimination • CMV (Cytomegalovirus) Also Decreases Expression Of MHC I • HIV (Human Immunodeficiency virus) Decreases MCH II Expression, No TH1 Support for CTL • Influenza Virus, Keeps Changing Antigens • Antigenic Drift • Antigenic Shift

  13. Bacterial Infections

  14. Bacterial Infections • Bacterial Infections Are Eliminated By Humoral Immunity • Exception: intracellular bacteria Ex. TB • DTH Is Important In Elimination Of Intracellular Bacteria • Antibodies Eliminate Bacteria Or Bacterial Toxins • Opsonization Of Bacteria • Neutralization Of Toxins • Exotoxins (Ex. Diptheria) • Endotoxins (Ex. LPS) • Lysis Of Bacteria Thru Complement Pathway • Complement Activation Thru Mast Cell Activation Results In Localized Inflammation • Vasodilation and Extravasation (Neutrophil Accumulation) • Bacteria Enter Host Thru • Respiratory Tract, GI Tract, Genitourinary Tract, Skin

  15. Bacteria Evade Host Defense Mechanisms • Bacterial Infection Involves 4 Steps • Attachment • Proliferation • Invasion Of Host Tissue • Toxin Induced Damage To Host Cells • Attachment • Some Bacteria Have Pili • Some Bacteria Secrete Adhesion Molecules (BordetellaPertussis) • Immune System Response To Attachment Is IgA • Prevents Attachment • Some Bacterial Evade IgA Thru Proteases That Decrease ½ Life Of IgA • Ex. HeamophilusInfluenzae • Some Bacteria Avoid Phagocytosis By Surrounding Themselves In A Polysaccharide Capsule. Ex. Streptococcus Pneumoniae

  16. Immune Response Against Pathogen Can Cause Pathogenesis • Overzealous Immune System Can Be Pathogenic • Bacterial Septic Shock • Predominant Cytokines Involved: IL-1 and TNF- • Source: M • Intracellular Bacteria Cause Granulomas • Extensive Tissue Damage • Ex. Tuberculosis • Tuberculosis (Mycobacterium Tuberculosis) • 3 Million Fatalities Every Year Globally • M Ingest M.T But Cannot Digest It • Eventually Burst Releasing Bacilli • M And TH1 Cells Form Granulomatous Lesion, Containment+Destruction Of Healthy Tissue • INF- and IL-12 Are Crucial In Eliminating Pathogen

  17. Immune Response to MTb • CD4+ T cells are activated within 2–6 weeks after infection. • Infiltration of large numbers of activated macrophages. • Wall off the organism inside a granulomatouslesion called a tubercle . • A tubercle consists of a few small lymphocytes and a compact collection of activated macrophages, which sometimes differentiate into epithelioid cells or multinucleated giant cells. • The massive activation of macrophages that occurs within tubercles often results in the concentrated release of lytic enzymes. These enzymes destroy nearby healthy cells, resulting in circular regions of necrotic tissue, which eventually form a lesion with a caseous (cheeselike) consistency • As these caseouslesions heal, they become calcified and are readily visible on x-rays, where they are called Ghon complexes.

  18. Protozoan Diseases • Protozoansare unicellular eukaryotic organisms:- • Amoebiasis, Chagas’ disease, African sleeping sickness, malaria, leishmaniasis, and toxoplasmosis. • The type of immune response that develops to protozoan infection and the effectiveness of the response depend in part on the location of the parasite within the host. • Many protozoans have life-cycle stages in which they are free within the bloodstream - humoralantibody is most effective. • Many of these same pathogens are also capable of intracellular growth- cell-mediated immune reactions are effective in host defense.

  19. Diseases Caused by ParasiticWorms (Helminths) • Unlike protozoans, which are unicellular and often grow within human cells, helminths are large,multicellularorganisms that reside in humans but do not ordinarily multiply there and are not intracellular pathogens. • Although helminths are more accessible to the immune system than protozoans, most infected individuals carry few of these parasites for this reason, the immune system is not strongly engaged and the level of immunity generated to helminthsis often very poor.

  20. SchistosomiasisMansoni • More than 300 million people are infected with Schistosoma, a trematode worm that causes a chronic debilitating infection. • Infection occurs through contact with free-swimming infectious larvae, called cercariae. • When cercariae contact human skin, they secrete digestive enzymes that help them to bore into the skin,where they shed their tails and are transformed into schistosomules. • The schistosomulesenter the capillaries and migrate to the lungs, then to the liver, and finally to the primary site of infection, which varies with the species. S. mansoni and S. japonicum infect the intestinal mesenteric veins.

  21. Immune Response against Viruses

  22. Immune Response against Bacteria

  23. Immune Response against Parasites/Worms

More Related