Immune System Flashcards
Natural Immunity (Innate resistance)
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.
Phagocytic cells
Neutrophils, macrophages, and dendritic cells.
Neutrophils
Present during acute inflammation and engulf microbes and kills them using cytoplasmic myeloperoxidase —> toxic to pathogens.
Macrophages
Derived from monocytes and leave the blood stream and differentiate into the tissues.
Dendritic cells
Engulf antigens in the epithelia of the skin, GI and respiratory tract.
Antigen Presenting Cells (APC)
Dendritic cells, macrophages, and B cells.
APC ingest and process antigens —> histocompatability complex II molecule and presented to the T-cell.
Natural killer cells
Contain granules that attack and kill virus-infected or cancerous cells
Complement cytokines
Collection of proteins which form a cascade of events to form the membrane attack complex
—> lyes a pathogen’s cell membrane
Acquired Immunity
Immunity that is obtained after exposure to an antigen.
Improves with repeated exposure and its specific.
Active acquired immunity
Produced by the host after exposure to an antigen or an immunization.
Basis of vaccines
Passive acquired immunity
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
Humoral immunity
Immunity conferred by B-Cells
Provides immunity against some viral infections, toxin induced diseases and diseases caused by pneumococci, meningococcal, and haemophilus.
Cell-mediated immunity
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
Bone marrow
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
Thymus
Shrinks but provides site for T- cell differentiation, maturation and selection.
Spleen
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
Lymph nodes, tonsils, and peyer’s patches
Site of antigen interact with immune cells
Peyer’s patches are lymph follicles in the mucus membrane that lines the small intestine.
CD4 cells, T-helper, or T4 cells
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
CD8 Cells, cytotoxic T-cells, killer T’s, T8 cells
Function to kill virus infected cells, tumor cells and allograft cells
By releasing cytotoxic chemicals that destroy the cell membrane or induce apoptosis.
Memory T-cells
Allows host to remember antigens and respond quicker and more vigorously after initial exposure.
Cells live for many years, can reproduce themselves.
T-regulatory cells
Slow or stop immune response once the invader is defeated
IgG
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.
IgE
Binds to mast cells, eosinophils, basophils
Involved in parasitic infections and hypersensitivity reactions
IgM
Produced early in the primary immune response
High levels of IgM —> recent infection
IgA
Main immune globulin in secretions and mucous membranes
Prevents attachment of microorganisms to mucous membranes
IgD
Found on the surface of B lymphocytes
Signals B cell activation
Autoimmunity
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.
Alloimmunity aka isoimmunity
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.
Primary immune response
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
Secondary Immune response aka Anamnestic response
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
Aging and the immune system
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
Fetal immunity
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
Neonate immunity
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
Allergic immune response
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)
SLE systemic lupus erythematosus
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.
Atopic disorders
Is when a person has a Type 1 reaction to the following hay fever, asthma, eczema and hives (urticaria)
Family Hx
Strong genetic predisposition
Rheumatoid Arthritis
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.
HLAs human leukocyte antigens
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
Organ rejection
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.
