The document discusses the two types of immune responses: cell-mediated (CMI) and humoral, detailing their mechanisms and phases. CMI involves T-cells and macrophages responding to intracellular pathogens, while the humoral response produces antibodies against foreign antigens. Key components include antigen processing, cytokine signaling, and the roles of various T-cell subsets and antibody classes in immunity.

1. Immune Responce
Samova Sanman
Samova.sanman@gmail.com

2. Cell Mediated immune Response
Humoral immne Responce
Two types

3. Cell Mediated immune
Response

4. Information
 Host defenses against extracellular infection are
mediated by: - Antibody
- Complement
- Macrophages
 Intercellular infections are mediates by CMI
 Cell mediated immune responce are responsible for:
- Resistance to intracellular pathogens
- Resistance to fungal and protozoal infections
- Resistance to tumors

5. CMI may play a role in some harmful conditions:
Hypersensitivity reactions type IV (contact dermatitis)
Graft rejection
Autoimmune diseases
Cell mediated Cytotoxicity mediated by:
T-cytotoxic cells
Natural killer cells
Activated macrophages

6. Characters Of CMI
Cellular immune response is mediated by:
 Subpopulation of T-lymphocytes
 Macrophages and their products

7.  Macrophages present antigen via their surface MHC to T-cells
 T-cells recognize antigen through their specific receptors (TCR)
 A specific T-cell clone becomes activated and begins to
proliferate
 Activated TH lymphocytes becomes effectors cells that secrete
cytokines

8. Characters Of Cellular immune response
Cytokines stimulate other effectors cells of CMI and humoral immune
response and mediate the following:
- Attract monocytes, macrophages and lymphocytes to the site
- Activate macrophages to kill intracellular microbes
- Promote activity of CD8 CTLs which directly kill virus infected cells, tumour
cells, and graft rejection
- They activate NK cells increasing their cytotoxic functions
- Stimulate B-cells to differentiate into plasma cells that secret antibodies

9. Phases Of Cell Mediated Immunity
1) Antigen processing and presentation
Protein antigens processed and converted to
peptides then bind to MHC molecules on Antigen
Presenting Cell (APCs ) to be presented to T-
cells

10. 1) Antigen Processing and Presentation
a- Extracellular proteins are internalized into vesicular
compartment of APCs (Dentritic, macrophages,B-cells)
- They are degraded to generate peptides
- These peptides bind into class II MHC molecules
- Peptide-MHC II complex is transported to surface
of APCs to be presented to CD4 TH cells (T Helper cell)
Outcome:
Secretion of cytokines by TH cells

11. b- Endogenously synthesized proteins are degraded to peptides (all
nucleated cells e.g virus infected cells)
- They bind to class I MHC in endoplasmic reticulum
- Peptide-MHC I complex is expressed on surface
of nucleotide cells to be represented to CD8
cytotoxic cells
Outcome:
Killing of presenting cells by CTLs

12. Activation of T-cells

13. * Mature CD4 and CD8 cells are activated by two signals:
- First signal is recognition of antigenic peptide-MHC complex
on surface of APC by TCR-CD3 complex
- CD4 and CD8 molecules are co-receptors that stabilize the
interaction of TH cells and TC-cells respectively with APCs
- CD3,CD4, and CD8 act as signal transduction molecules
- Second co-stimulatory signal is:
interaction of CD28 on T-cells with CD7 on APCs

14. * TH-cells express IL-2 receptors and secrete cytokines including
IL-2
* IL-2 auto activate TH-cells
* APC release IL-I which acts on both APC and TH cell to promote
their activation
* All mentioned interactions lead to activation of mature TH-cells
* Mature TH-cells proliferate and differentiate into effectors antigen
specific TH-cells releasing cytokines
* Some of them become memory cells which provide secondary
immune response
* Cytokine released from activated TH-cells activate macrophages,
NK and B-cells

15. Phases Of Cell Mediated Immunity

16. * Activated CD8 TC-cells proliferate and differentiate into a
clone of effectors cells CTLs
* Effectors CTLs kill target cells
i.e. nucleated cells (expressing MHC-I) infected with
viruses, tumor cells or graft cells

17. Activation of Macrophages and Delayed Type
Hypersensitivity (DTH)
Activated TH cells (TH1) secrete IFN-γ which
activates macrophages and increase their ability to kill
ingested intracellular pathogens

18.  The process of activation of macrophages, NK cell
and cytotoxic T-cells, infiltration and proliferation of
inflammatory cells, stimulated by cytokines released
from TH-cells (TH1) is important protective
mechanism against intracellular pathogen

19. Activated macrophages can also kill abnormal host cells
(abnormal or tumor cells)
Its Cytotoxicity is non specific and stimulated by TNF, nitric
oxide, enzymes and oxygen metabolites
If infection is not fully resolved, activated macrophages
cause tissue injury and fibrosis i.e. DTH reaction

20. Humoral Immune Response

21. Results in production of proteins called
“immunoglobulins” or “antibodies”.
Body exposed to “foreign” material termed
“antigen” which may be harmful to body: virus,
bacteria, etc.
Antigen has bypassed other protective
mechanisms, ie, first and second line of
defense.

22. Dynamics of Antibody Production
 Primary immune response
 Latent period
 Gradual rise in antibody production taking days to
weeks
 Plateau reached
 Antibody level declines

23.  Antibody production
 Initial antibody produced in IgM
 Lasts 10-12 days
 Followed by production of IgG
 Lasts 4-5 days
 Without continued antigenic challenge
antibody levels drop off, although IgG
may continue to be produced.

24. Secondary Response
 Second exposure to SAME antigen.
 Memory cells Have memory of the antigen.
 Recognition of antigen is immediate.
 Results in immediate production of
protective antibody, mainly IgG but may see
some IgM

27. Cellular Events
Antigen is “processed” by T lymphocytes and
macrophages.
Possess special receptors on surface.
Termed “antigen presenter cell” APC.
Antigen presented to B cell

28. Basic Antibody Structure
Two identical heavy chains
 Gamma
 Delta
 Alpha
 Mu
 Epsilon
Two identical light chains
 Kappa OR
 Lambda

30. Papain Cleavage
 Breaks disulfide bonds at hinge region
 Results in 2 “fragment antigen binding” (Fab)
fragments.
 Contains variable region of antibody molecule
 Variable region is part of antibody molecule which
binds to antigen.

31. Pepsin
 Breaks antibody above disulfide bond.
 Two F(ab’)2 molecules
 The rest fragments
 Has the ability to bind with antigen and cause
agglutination or precipitation

33. IgG
 This monomer is the most abundant and diverse accounts
for about 80-85% of allantibodies.
 These monomers can crosses the placenta and confers
passive immunity, as well as, blood vessels.
 Monomers activate complement and increase
phagocytosis.
 These monomers convey long term immunity
 IgG protect against circulating bacteria and viruses, and
bacterial toxins.

34. IgM
 This monomer comprises about 5-10% of the antibodies
in serum.
 IgM are the first ones to appear in response to the initial
exposure to an antigen.
 IgM have a pentamer structure.
 They large size prevent IgM from moving about as
freely as IgG, therefore, they remain in the blood
vessels.
 They fix complement

35. IgA
 This monomer accounts for about 15% of the
antibodies in serum.
 IgA can be monomers or dimers.
 IgA monomers are found in salvia, sweat, breast
milk, and secretions of the G.I. tract.
 They do not fix complement
 The main function of IgA is to prevent the
attachment of pathogens to mucosal surfaces.

36. IgD
 IgD atibodies comprise only about 0.2% of the total
serum antibodies.
 IgD antibodies are found in blood and lymph and on
the surfaces of B cells.
 They do not fix complement.
 They help to initiate the immune response.

37. IgE
 IgE antibodies comprise about 0.002% of the total
number of antibodies.
 IgE molecules bind tightly by their Fc ends to
receptors on mast cells and basophils. This causes
the release of histamine.
 They do not fix complement.

39. PRIMARY and SECONDARY
INFECTION

40. 1. Primary response – after first exposure to an
Ag immune system produces IgM and a
gradual increase in Ab titer.
2. Secondary response –after second contact
with the same Ag, immune system produces
a more rapid, stronger response due to
memory cells.

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