Exam 1 results

1
Exam 1 results
Average 78.05
2
Opening image
3
Figure 12.1Page 414
Adenoid
Tonsil
Thymus
Peyers patches in small intestine (gut-associated
lymphoid tissue)
Lymph node
Spleen
Lymphatic vessel
Appendix
Bone marrow
4
Figure 12.2Page 417
Bacterial invasion or tissue damage
Release of histamine by mast cells
Increased local capillary permeability
Local arteriolar vasodilation
Increased blood delivery to injured tissue
Local accumulation of fluid
Redness
Swelling
Pain
Heat
Increase in crucial plasma proteins, such as
clotting factors, in tissue
Increase in phagocytes in tissue
Phagocytic secretions
Defense against foreign invader tissue repair
Systemic responses, such as fever
5
Figure 12.3Page 418
Blood capillary
Leukocyte leaving capillary
6
Figure 12.4Page 418
Bacterium
Activated complement molecule, C3b (an opsonin)
Receptor specific for activated C3b molecule
Phagocyte
Structures are not drawn to scale.
7
Figure 12.5Page 419
(release)
Neutrophils
Kallikrein
Kininogens
Kinins
(attract)
Promote localized vasodilation and increased
capillary permeability
Activate pain receptors
Stimulate complement system
Act as chemotaxins
8
Figure 12.6 (1)Page 420
9
Figure 12.6 (2)Page 421
10
Figure 12.7Page 422
Virus enters a cell
First cell invaded by a virus
Cell releases interferon
Interferon binds with receptors on uninvaded
cells
Uninvaded cells produce inactive enzymes
capable of breaking down viral messenger RNA and
of inhibiting protein synthesis
Virus enters cell that has been acted upon by
interferon
Subsequent cells invaded by a virus
Virus-blocking enzymes are activated
Virus is unable to multiply in newly invaded cells
11
Figure 12.8Page 423
C9
C5b6
C7
C8
12
Figure 12.9Page 424
Red blood cells Platelets Monocytes Granulocytes
Bone marrow
Hemopoietic precursor cell
Bone marrow lymphocyte
Thymus
T cells
B cells
Peripheral lymphoid tissues
Foreign invasion
B cells
T cells
Antibody-mediated immune response
Cell-mediated immune response
13
Figure 12.11Page 426
Antigens
Specific antigen- binding sites
Fab
Light chain
Fc
Heavy chain
Antibody
14
Fig. 12.12 (1)Page 427
Neutralization
Invading bacterium
Bacterial toxin
Antibody neutralizing toxin
Antibody specific to toxin
15
Fig. 12.12 (2)Page 427
Agglutination (clumping of antigenic cells) and
precipitation (if soluble antigen-antibody complex
is too large to stay in solution)
Foreign cells (e.g., transfused mismatched red
blood cells)
Antigen
Lattice
Antibodies specific to foreign cells
16
Fig. 12.12 (3)Page 427
Activation of complement system
(binds with)
Inactive C1 complement molecule
Antibody
Antigenic foreign cell, such as invading bacterium
Activated by binding with antigen-attached
antibody
(leads to)
Formation of C5C9, the membrane-attack complex
(forms holes in foreign cell)
Lysis (rupture) of cell
Membrane-attack complex
17
Fig. 12.12 (4)Page 427
Enhancement of phagocytosis (opsonization)
Invading bacterium coated with antibodies specific
to it
Phagocyte
18
Fig. 12.12 (5)Page 427
Stimulation of killer cells
Invading bacterium coated with antibodies specific
to it
Lysis induced by killer cell
Killer cell
19
Figure 12.13Page 429
B cell specific to antigen
Different B cell clones
Antigens
Rough endoplasmic reticulum
Memory cells
Plasma cells
Antibodies
20
(No Transcript)
21
Fig. 12.14aPage 430
Primary immune response
Time of first exposure to microbial antigen
22
Fig. 12.14bPage 430
Secondary immune response
Time of subsequent exposure to microbial antigen
23
Figure 12.15Page 431
First exposure to a pathogens antigens
Natural exposure to virulent, antigenic pathogen
Exposure to nonvirulent, antigenic
pathogen through vaccination
Virulent portion
Antigenic portion
No virulence
Combat
Disease
Specific B cell clone
Specific B cell clone
No disease
Plasma cells
Memory cells (long-term immunity)
Memory cells (long-term immunity)
Plasma cells
Antibodies (slow, weak primary response)
Antibodies (not needed)
Subsequent exposure to same virulent pathogen
Plasma cells
Plasma cells
Combat
Combat
Antibodies (swift, strong secondary response)
Antibodies (swift, strong secondary response)
No disease
24
Fig. 12.16 (1)Page 433
Donor type B blood
Recipient with type A blood
Antigen B
Antibody to type A blood
Antigen A
Antibody to type B blood
(See next slide)
25
Fig. 12.16 (2)Page 433
Red blood cells from donor agglutinate
Clumping blocks blood flow in capillaries
Red blood cells usually burst
Oxygen and nutrient flow to cells and tissues
is reduced
Hemoglobin precipitates in kidney, interfering
with kidney function
26
Figure 12.17Page 434
Invading bacteria
Macrophages secrete interleukin 1, which
enhances B cell proliferation and antibody
secretion
Macrophages process and present bacterial
antigen to B and T lymphocyte clones specific
to the antigen
Interleukin 1
Macrophage
Helper T cell
B cell
Antibodies enhance phagocytosis by coating the
bacteria and serving as opsonins
Activated helper T cell
Helper T cells secrete B cell growth factor that
enhances B cell proliferation and
antibody secretion
B cell growth factor
Plasma cell
Plasma cells secrete antibodies that bind with
the antigenic bacteria
Antibodies
27
Fig. 12.19 (1)Page 437
Virus
Viral antigenic protein coat
Host cell
Self-antigen
A virus invades a host cell.
28
Fig. 12.19 (2)Page 437
Foreign viral antigen
Self-antigen
Virus-invaded host cell
The viral antigen is displayed on the surface of
the host cell alongside the cells self-antigen.
29
Fig. 12.19 (3)Page 437
Cytotoxic T cell
T cell receptor
Self-antigen and foreign antigen complex
Virus-invaded host cell
The cytotoxic T cell recognizes and binds with a
specific foreign antigen (viral antigen) in
association with the self-antigen.
30
Fig. 12.19 (4)Page 437
The cytotoxic T cell releases chemicals that
destroy the attacked cell before the virus can
enter the nucleus and start to replicate.
31
Fig. 12.20aPage 438
Granule containing perforin molecules
Killer cell
Target cell
Perforin molecule
Granule
Salt, H2O
Killer cell
Ca2
Target cell
32
Fig. 12.20bPage 438
Perforin molecule
33
Figure 12.21Page 442
Cytotoxic T cell
T cell receptor
Foreign antigen
MHC self-antigen
Invaded cell
34
Fig. 12.22 (1)Page 442
Class I MHC glycoproteins
Found on surface of all cells
Recognized only by cytotoxic T cells
Cytotoxic T cells can destroy body cells if
invaded by foreign (viral) antigen
35
Fig. 12.22 (2)Page 442
Class II MHC glycoproteins
Found on surface of special immune cells (B
cells, cytotoxic T cells, and macrophages)
Recognized only by helper T cells
Helper T cells enhance activities of these
immune cells when they are combating
antigenic invaders
36
Figure 12.24 Page 444
Inhibits multiplication of cancer cells
Interferon
Enhances
Secretes
Enhances
Enhances
Secretes
Secretes
Cytotoxic T cell (prior exposure to cancer cell)
Natural killer cell
Macrophage
Phagocytosis
Toxic chemicals
Directly attack and destroy cancer cells
Start here
37
Fig. 12.26 (1) Page 448
Allergens
Specific B cell clones
38
Fig. 12.26 (2) Page 448
Activated plasma cells
39
Fig. 12.26 (3) Page 448
IgE antibodies
Granule filled with histamine
IgE tail receptor
Mast cell
Allergic response
Histamine and other chemicals
40
Figure 12.27 Page 449
Smooth muscle
Sweat pore
Sebaceous gland
Melanocyte
Langerhans cell
Keratinized layer
Living layer
Hair shaft
Epidermis
Keratinocyte
Granstein cell
Dermis
T lymphocyte
Hypodermis
Adipose cells
Nerve fiber
Hair follicle
Pressure receptor
Sweat gland
41
Figure 43.10 An overview of the immune responses
(Layer 1)
42
Figure 43.10 An overview of the immune responses
(Layer 2)
43
Figure 43.10 An overview of the immune responses
(Layer 4)
44
(No Transcript)
45
(No Transcript)
46
(No Transcript)
47
Progression of Crohns Disease
48
(No Transcript)
49
(No Transcript)
50
(No Transcript)