1. Immune Response to Infection

2. Infectious Agents
Viruses
Bacteria
Parasites
Protozoa

6. Primary response: Natural Killer Cells: Macrophages:
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.

7. 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.

8. Tertiary response: Cytotoxic T Cells: Antibodies:
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.

9. Viral Infections

10. Overall Response to Viral Infections

11. Innate Immune Response

12. 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
Ag-MHC I
CD8 T cell
CTL
virus
infection
Ag-MHC II
CD4 T cell
TH1
IL12
IFN-
Viral antigen
Endocytosis
Pinocytosis
phagocytosis
TH1 failitates CD8 T cell
activation by producing IL2
and activation of DCs
through CD40L-CD40

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

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

15. 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

16. Bacterial Infections

17. 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

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

21. 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

22. 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 granulomatous lesion 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 caseous lesions heal, they become calcified and are readily visible on x-rays, where they are called Ghon complexes.

24. Protozoan Diseases Protozoans are 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 - humoral antibody is most effective.
Many of these same pathogens are also capable of intracellular growth- cell-mediated immune reactions are effective in host defense.

26. Diseases Caused by Parasitic Worms (Helminths)
Unlike protozoans, which are unicellular and often grow within human cells, helminths are large,multicellular organisms 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 helminths is often very poor.

27. Schistosomiasis Mansoni
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 schistosomules enter 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.

29. Immune Response against Viruses

30. Immune Response against Bacteria

31. Immune Response against Parasites/Worms