1. People will forget what But people will never forget
you said,
people will forget
what you did,
But people will never forget
how you made them
feel.
Maya Angelou

2. Immune system
Defense against bacteria, viruses, foreign matter.
Generally protective BUT can be adverse if: - response is excessive
- attacks self

3. Innate Immunity - rapid response
Always present
In place before anything happens
Attacks non-self microbes
Does NOT establish memory
Does not distinguish between different microbes
Mechanisms include:
Epithelial barriers
Phagocytic cells – Neutrophils/Macrophages
Natural killer cells
Plasma proteins

4. Adaptive Immunity – slower but lethal
Develops a memory
Returning microbes are attacked so quickly the patient is usually unaware they are even there.
Consists of:
T and B lymphocytes
Antibodies
Triggered by Antigens…..

5. Adaptive Immunity – two types:
Attacks specific microbes (antigens)
Humoral immunity – B lymphocytes (antibodies- proteins in the blood that attack the specific antigen) Extracellular microbes
Cell-mediated immunity (phagocytic cells that attack the specific intracellular antigen)

6. Antibodies or Immunoglobulins
IgG: circulates in body fluids, passed from mom to baby…
IgM: circulates in body fluids; biggest/first to appear
IgE: found on mast cells in tissues; present w/inflammation, allergies and parasites
IgA: found in secretions on mucus membranes; prevents antigens from entering the body
IgD: found on the surface of B cells; acts as an antigen receptor

7. Cell-mediated Defends against intracellular microbes by T-lymphocytes
Regulatory cells control the immune response
T helper cells – recognize self versus non-self - rejection
T suppressor cells – shuts response down – CD4s regulate
Antigen presenting cells - macrophages
Effector cells then carry out the attack on the antigen
T cytotoxic (or T killer) cells – trigger apoptosis
B cells (produce antibodies) - humoral
Leukocytes – phagocytes – macrophages….

8. Ability to recognize self
Innate and adaptive responses work together
Key to immune response
Uses HLA receptors on the MHC molecule of cells
Human Leukocyte Antigens
Major Histocompatibility Complex molecules
Called autoimmune disease if body attacks ‘self’ cells

9. Lewis Fig 14-2 pg 205

10. CELLS OF IMMUNE SYSTEM All come from the bone marrow:
Macrophages (monocytes)
Phagocyte
Antigen presenting cell
Neutrophils
phagocyte

11. CELLS OF IMMUNE SYSTEM Lymphocytes – key to adaptive B’s
Antigens cause differentiation
Produce antibodies (humoral immunity)
Bind to microbes and prevent colonization
T’s
Control cell-mediated immunity
Create:
Helper T-cells and Cytotoxic T-cells
Classified by surface proteins
CD4 and CD8

12. Tissues of Immune System
Bone Marrow-
Cell production
B-cells maturation
Thymus-
T-cells mature here
Begins to shrink at puberty
Can be re-activated if needed.

13. Selection!
ONLY the T-cells and B-cells that are able to recognize self from non-self are allowed to mature and then are released into circulation.
This is highly critical with regard to autoimmune diseases

14. Tissues of Immune System
Lymph nodes-
Axillae, groin, neck, thorax, abdomen
Remove foreign matter
Proliferate immune cells
Collects fluid from tissues
Spleen-
Filters antigens from blood
B’s and T’s hang out here
Processes antigens

15. MHC contain HLA
Major Histocompatibility Complex molecules contain Human Leukocyte Antigens
This molecule involved in self-recognition
T-lymphocytes activated or not by recognizing HLA
Key to organ/tissue rejection
Key to immune regulation
Everyone has unique HLAs

16. Active versus Passive Active: Either have the disease or immunized
Long lasting!
Responds quickly w/subsequent exposures
Passive:
From another source
Mom passes IgG antibodies to infant
Immunoglobin are antibodies from another person which can be injected into exposed individual.
Short term!

17. Disorders of Immune Response:
Includes:
Hypersensitivity
Transplant rejections
Autoimmune diseases
Immunodeficiencies

18. Hypersensitivity – 4 types
Excessive or inappropriate activation of the immune response
The body is damaged by the immune response, rather than by the allergen.
Discussion:
How many different allergies do the members of this class have?
What are their common signs and symptoms?
Can the general process of inflammation explain these signs and symptoms?

19. Type I Hypersensitivity - IgE
Commonly called “allergic reactions”
Antigens are called allergens
Local or atopic reactions (genetic)
Hives (urticaria),Rhinitis (hay fever),Food allergies
Contact (Atopic) dermatitis

21. Type I Hypersensitivity
Debilitating - Bronchial asthma
Systemic and life-threatening: anaphylaxis
Widespread edema - What would this cause?
Difficulty breathing
Vascular shock from vasodilation
S/S: itching, hives, skin erythema
Bronchospasm
GI issues
Treat w/epi, stabilize airway – get help!

22. Type I Hypersensitivity
First exposure to allergen = sensitization
Usually a limited or no response –
Primes immune system (memory formed)
Next exposure:
Mast cells degranulate and triggers massive inflammatory response which causes damage
Not all IgE responses cause disease or damage

23. Type II Hypersensitivity - antibody
Cytotoxic – cells are coated w/antibodies which attracts phagocytes
IgG or IgM attack antigens on cell surfaces
Usually involves antigens on red or white blood cells
Transfusion reactions
Rh disease
Drug reactions

24. Scenario A woman is RH-negative and her husband is Rh-positive.
She is pregnant with their first child and the doctor has prescribed RhoGAM, but the woman is confused about this .
She says she does not want to take any drugs while she is pregnant—and besides, the doctor told her that her first child was not at much risk for Rh disease.
Question:
Why can’t she wait to take RhoGAM if she gets pregnant again and really needs it?

25. Question
Why is type O blood considered the universal donor?
A. It has both A and B antigens on the RBC.
B. It has neither A or B antigens on the RBC.
C. It has no antibodies in the plasma.
D. It has A and B antibodies in the plasma.

26. Answer B. It has neither A or B antigens on the RBC.
Antigens are the components that elicit an immune response (type II hypersensitivity reaction). Type O blood has no antigens on the RBC, so anyone can receive it because there is nothing to stimulate production of antibodies against it. The fact that type O blood has both A and B antibodies has nothing to do with creating the antigen-antibody response.

27. Type II Hypersensitivity – antibody continued:
Antibodies deposited in tissues causes Inflammatory response:
Glomerulonephritis; transfusion or organ/graft rejections
Autoantibodies:
Target “self” cells – very specific ones
Examples: Graves disease and myasthenia gravis

28. Type III Hypersensitivity – antigen/antibody complexes
Free-floating antigen + antibody 
circulating immune complex
Systemic Lupus Erthematosus (SLE) RA
Glomerulonephritis
Triggers: antibiotics, drugs, foods, insect venom

29. Mechanism of Type III Hypersensitivity
Immune complexes deposit on walls of blood vessels and activate complement
Tissues are damaged
Author: Add text?

30. Question
Administration of certain antibiotics may result in type III sensitivity reaction.
A- True
B- False

31. Answer
True
A side effect associated with antibiotic administration (especially penicillin) is serum sickness, which may cause a type III hypersensitivity reaction.

32. Type IV Hypersensitivity – cell mediated
Cell-mediated: sensitized T cells attack antigen
Direct cell-mediated cytotoxicity
Attacks specific MHC markers
Delayed-type hypersensitivity
Tuberculin test

33. Transplant Rejection
Graft: cells, tissues, organs from donor to recipient
Autologous – donor and recipient = same person
Allogenic – donor different person
Surface antigens (MHC/HLA) are present:
Rejection based on how closely these are matched

34. Circulating antibodies react with graft Acute- months to years
Transplant Rejection
Hyperacute- very fast!
Circulating antibodies react with graft
Acute- months to years
Exposure to transplant causes activation of immune system, especially T cells
Chronic – prolonged - slow
Blood vessels in transplant gradually damaged
Author: Next slide says graft-vs-host; are they the same?

35. Autoimmune Diseases
Immune system attacks self-antigens
Normally, self-reactive immune cells are killed in the lymphoid organs or suppressed by regulatory T cells.
B-Cells develop antibodies against self
T-Cells see self as foreign

36. Autoimmune Diseases Suspected triggers:
Viruses, chemicals, microorganisms
Inheritance plays a role
Diagnosing:
Evaluation of S/S while r/o other causes
ELISA or IFA show antibodies
Treatment:
Focus is on trigger –
Corticosteroids and immunosuppressant's

37. Question
Patients who suffer from autoimmune disease have hypoactive immune systems.
True
False

38. Answer
False
In autoimmune diseases, the immune system is hyperactive—it attacks self-antigens and destroys its own body tissues.

39. Immunodeficiency Primary- congenital or inherited B-cell deficiencies
Antibody deficiencies
T-cell deficiencies
Combined immunodeficiencies
Secondary – acquired later in life
More common than primary
AIDS

40. HIV Infects a Cell HIV is a retrovirus that attacks the CD4 t-cells.
Author: Add text?

41. Course of HIV Infection
Primary infection phase
Signs of systemic infection
Seroconversion: immune system responds and antibodies against HIV appear (1–6 months)
Latent period
Virus is replicating, CD4 cell count gradually falls
May last 10–11 years or longer
Overt AIDS
CD4 cell count <200 cells/mL or AIDS-defining illness

42. Human Immunodeficiency Virus
Transmitted by blood and body fluids
Sexual contact
Breast milk, vaginal secretions
Blood-to-blood contact
Contaminated needles
Occupational – universal precautions
Transfusions – screenings began in 1985
Individual is infectious even w/NO signs or symptoms

43. AIDS-Associated Illnesses
Opportunistic infections
Respiratory – Tb leading cause of death
Gastrointestinal -GI
Nervous system – CNS
Malignancies – Kaposi sarcoma and non-Hodgkins lymphoma
Treatments:
Anti-retroviral interrupts the life cycle
Reverse transcriptase inhibitors interrupts replication cycle

44. In Class activity

45. Next week – exam 2
Homework
Genetics
Lewis ch 13

46. Create your own
Visual image of
Inflammation and
Immune response
Starting point:
Splinter w/strep