Immune System

Question 1

Natural Immunity (Innate resistance)

Answer 1

Resistance that exist prior to exposure to a microbe.

Born with it, based on our genotype and species.

Involves nonspecific barriers such as: skin, mucous membranes, NK cells and complimentary cytokines proteins, inflammation, and phagocytosis.

Function: to kill invading microorganisms and activates acquired immunity.

Cells in natural immunity: phagocytosis cells, antigen presenting cells, natural killer cells and complement.

Question 2

Phagocytic cells

Answer 2

Neutrophils, macrophages, and dendritic cells.

Question 3

Neutrophils

Answer 3

Present during acute inflammation and engulf microbes and kills them using cytoplasmic myeloperoxidase —> toxic to pathogens.

Question 4

Macrophages

Answer 4

Derived from monocytes and leave the blood stream and differentiate into the tissues.

Question 5

Dendritic cells

Answer 5

Engulf antigens in the epithelia of the skin, GI and respiratory tract.

Question 6

Antigen Presenting Cells (APC)

Answer 6

Dendritic cells, macrophages, and B cells.

APC ingest and process antigens —> histocompatability complex II molecule and presented to the T-cell.

Question 7

Natural killer cells

Answer 7

Contain granules that attack and kill virus-infected or cancerous cells

Question 8

Complement cytokines

Answer 8

Collection of proteins which form a cascade of events to form the membrane attack complex

—> lyes a pathogen’s cell membrane

Question 9

Acquired Immunity

Answer 9

Immunity that is obtained after exposure to an antigen.
Improves with repeated exposure and its specific.

Question 10

Active acquired immunity

Answer 10

Produced by the host after exposure to an antigen or an immunization.

Basis of vaccines

Question 11

Passive acquired immunity

Answer 11

Immunity acquired via the transfer of antibodies or T-cells to the recipient.

Natural passive acquired immunity
- mother to baby in breast milk or via placenta

Artificial passive acquired immunity
-antibodies are given to a recipient to provide immunity
-ex: rabies, tetanus, hepatitis, and snake bites.
-good way to fight infection, immediate protection, immunity only last 2 weeks

Question 12

Humoral immunity

Answer 12

Immunity conferred by B-Cells
Provides immunity against some viral infections, toxin induced diseases and diseases caused by pneumococci, meningococcal, and haemophilus.

Question 13

Cell-mediated immunity

Answer 13

Immunity conferred by T-Cells.

Immunity active against cells infected with intracellular bacteria or viruses.

Defends against CA, fungal infections, parasitic infections, tumors and is responsible for organ transplant rejection

Question 14

Bone marrow

Answer 14

Responsible for production of immune cells and maturation of B cells

Red pulp: location of RBC storage and turnover

White pulp: immune cell interactions occur

Question 15

Thymus

Answer 15

Shrinks but provides site for T- cell differentiation, maturation and selection.

Question 16

Spleen

Answer 16

Lymphoid organ

Contains blood filled sinuses which filter antigens and cells from the blood

Red pulp: RBC storage and turnover

White pulp: site where immune cell interaction occur, APC present to the lymphocytes of the spleen —> trigger immune response

Spleen problems? Splenectomy or sickle cell anemia
-increased risk of streptococcal bacteria infections
—> need the pneumococcal vaccine

Question 17

Lymph nodes, tonsils, and peyer’s patches

Answer 17

Site of antigen interact with immune cells

Peyer’s patches are lymph follicles in the mucus membrane that lines the small intestine.

Question 18

CD4 cells, T-helper, or T4 cells

Answer 18

Function to activate macrophages, B-cells, cytotoxic T-cells, and other CD4 cells.

Release lymphokines that begin the inflammatory process
Role in mediating delayed hypersensitivity reactions (TB skin test) by TH1 and TH2

Question 19

CD8 Cells, cytotoxic T-cells, killer T’s, T8 cells

Answer 19

Function to kill virus infected cells, tumor cells and allograft cells

By releasing cytotoxic chemicals that destroy the cell membrane or induce apoptosis.

Question 20

Memory T-cells

Answer 20

Allows host to remember antigens and respond quicker and more vigorously after initial exposure.

Cells live for many years, can reproduce themselves.

Question 21

T-regulatory cells

Answer 21

Slow or stop immune response once the invader is defeated

Question 22

IgG

Answer 22

Most prominent, binds with viruses, bacteria, and toxins.
Activates the complement and binds to macrophages, primary antibody in the secondary immune response.
Levels increases with each follow up infection and levels rise at the end of a primary infection

Only immunnogobulin that passes the placenta.

Question 23

IgE

Answer 23

Binds to mast cells, eosinophils, basophils
Involved in parasitic infections and hypersensitivity reactions

Question 24

IgM

Answer 24

Produced early in the primary immune response

High levels of IgM —> recent infection

Question 25

IgA

Answer 25

Main immune globulin in secretions and mucous membranes Prevents attachment of microorganisms to mucous membranes

Question 26

IgD

Answer 26

Found on the surface of B lymphocytes Signals B cell activation

Question 27

Autoimmunity

Answer 27

Immunity misdirected against the host’s own cells Is a disturbance in the immunologic tolerance of self-antigens. Autoimmunity can cause autoimmune disease when the immune system reacts against self-antigens to such a degree that the person’s own tissues are damaged by autoantibodies or autoreactive T cells.

Question 28

Alloimmunity aka isoimmunity

Answer 28

Occurs when the immune system of one individual produces a reaction against tissues of another individual Can be observed during immunologic reactions against transfusion, transplanted tissue, or the fetus during pregnancy.

Question 29

Primary immune response

Answer 29

Initial and 1st exposure to an antigen Occurs within 5-7 days after exposure to antigen Increase in IgM and later an increase of IgG antibodies

Question 30

Secondary Immune response aka Anamnestic response

Answer 30

Occurs with second exposure of an antigen Marked increase of IgM and even more earlier increase of IgG antibodies Stronger immune response to prior exposed antigen

Question 31

Aging and the immune system

Answer 31

Immune function decreases with age After 60, decrease in T-cell activity Middle age thymus is only 15% of maximum size —> decrease in T-cell differentiation. T-cell numbers DO NOT decrease B-cells produce less antibodies in response to invading antigens and there is a decrease in memory B-cells Increase in autoantibodies

Question 32

Fetal immunity

Answer 32

Able to make a primary response and secret IgM antibodies Cannot make its own antibodies (IgG or IgA) uses mom’s antibodies that pass throw the placenta

Question 33

Neonate immunity

Answer 33

Immature newborn immunity Deficient phagocytic activity, antibody production and complement activity. IgG levels increase at 5-6 months to adult levels. Newborns don’t make any IgG or IgA antibodies

Question 34

Allergic immune response

Answer 34

Type 1 immediate hypersensitivity response to an environmental antigen. ex: food,medication, pollen. Mediated by IgE Antigen —binds —> IgE (priming for later rxn to occur) = antigen-IgE complex Antigen round 2 —binds to antigen-IgE complex —> detected by mast cells Mast cells —> degranulation —> histamine and triggers the inflammatory response. S/S: hives, Angioedema, asthma exacerbation, anaphylaxis, hypotension, shock, death. Treatment: steroids, hydration and epinephrine (dilation of bronchial smooth muscle)

Question 35

SLE systemic lupus erythematosus

Answer 35

Chronic multi-system inflammatory disease who is genetically predisposed to autoimmunity Common in African American women and women ages 20-40 The body forms antibodies against itself via cellular components ex: DNA, RNA, histones, erythrocytes, nucleic acids, coagulation proteins, phospholipids, lymphocytes, platelets. Antibody-antigen complexes are deposited into a variety of tissues: kidneys, lungs, joints, skin and blood vessels. —> activates the complement and inflammatory response S/S: butterfly rash, photosensitivity, arthritis, inflammation of serous sacs (pericardial or pleural sacs) pulmonary hemorrhage, proteinuria, seizures, anemia, thrombocytopenia.

Question 36

Atopic disorders

Answer 36

Is when a person has a Type 1 reaction to the following hay fever, asthma, eczema and hives (urticaria) Family Hx Strong genetic predisposition

Question 37

Rheumatoid Arthritis

Answer 37

Systemic autoimmune disease that causes chronic inflammation of connective tissues primarily joints. Most common in women, incidence increases with age over 30 IgM autoantibodies are formed against IgG antibodies IgM —bind—> IgG —> antigen antibody complex that deposit into synovial membranes causing membranes to infiltrate with T-cells, plasma cells and Macrophages —> immune system response S/S: joint inflammation, pain, deformity and disability, swelling, erythemic joints, morning stiffness, wt loss, weakness, and anorexia. Extra synovial rheumatoid nodules may be present and can be invasive in the cardiac valves, pericardium, pleura, lung parenchyma, and spleen. HLA-DRB1 gene associated with an increase risk of developing RA Risk factors: smoking, smoking mothers, nulliparity, obesity, low SES, women, over 60 years old.

Question 38

HLAs human leukocyte antigens

Answer 38

MHC molecules or HLAs molecules Humans have two HLAs one inherited from each parent that are codominately expressed on each cell HLA genes have multiple forms of expression on the loci of a cell Sibling donor matches are only 25% possible

Question 39

Organ rejection

Answer 39

Hyperacute rejection (rare) -happens immediately after transplantation, when circulation is established to the graft area and the organ turns white instead of pink. Usually occurs if recipients already of preexisting antibodies to HLA antigens, prior blood transfusion, multiple pregnancies (antigens against husbands blood) —> inflammatory response —> coagulation cascade = no tissue perfusion Acute rejection -cell mediated immune response that occurs days to months after transplantation. This type of rejection occurs when the immune system developes antibodies against unmatched HLAs after transplantation. Recipients lymphocytes interact with donor’s dendritic cells —> recipient releases cytotoxic T cells and attack donor tissues. Immunosuppressive drugs may delay or lessen intensity of acute rejection Chronic rejection - may occur after months or years of normal function, slow progressive organ failure. Causes by weak cell mediated immune response.