An agent that promote developmental anomalies (e.g. drugs, alcohol, heavy metals, physical trauma, viral/bacterial infections)
What are the variables associated with teratogens?
Host susceptibility, embryological stage of exposure, tissue specificity, dose dependency
What are some of the malformations associated with diabetes?
Limb deficiency, heart defects, holoprosencphy, heterotaxy
Involution failure describes what type of morphogenetic error?
Persistence of embryologic tissue
Atresia describes what type of morphogenetic error?
Incomplete formation of lumen
Dysplasia describes what type of morphogenetic error?
Disorganized cell development
Ectopia, or heterotopia, describes what type of morphogenetic error?
Organ development in an abnormal site
Choristoma describes what type of morphogenetic error?
Normal tissue in an abnormal site
Microdontia is a type of hypoplasia that describes what structure as smaller than normal?
Micrognathia is a type of hypoplasia that describes what structure as smaller than normal?
The thryoglossal duct cyst, the persistence of embryologic thyroid tissue outward visible, is an example of what morphogenetic error?
The spina bifida subtype meningocele is the mildest, characterized by an abnormal tuft of hair, hemangioma, and a mild dysraphic anomaly. True or false?
Ingestion of what supplement/vitamin would prevent spina bifida during pregnancy?
Clinical features, including microcephaly, focal cerebral calcifications, cataracts, lung disease, petechiae/purpura, are indicative of what type of pathology?
What is the leading cause of death in the first year of life?
What is the leading cause of death for children aged 4-14 years?
What is the second leading cause of death for children aged 4-14 years?
An overgrowth of normal tissue in a normal site is what type of cancer?
What is the most frequent benign tumor found in childhood?
Disease caused by chronic exposure to alcohol during pregnancy. Clinical features include growth retardation, CNS dysfunction, epicanthal folds, short palpebral fissures, max/man hypoplasia, thin upper lip, poorly developed philtrum, some heart cardiac se
Fetal alcohol syndrome
Disease caused by various congenital infections. Clinical features include microcephaly, focal cerebral calcification, eye issues, lung disease, heart disease, splenomegaly, petechiae/purpura, jaundice.
Disease resulting from incomplete closure of spinal cord or vertebral column. Can be prevented by folic acid supplements. Some possible features: leg weakness/paralysis, bowel/bladder problems, seizures, deformed feet, uneven hips, scoliosis; abnormal hai
Autosomal dominant disease. Features typically include elevated serum LDL, early heart disease, increased risk of stroke, atherosclerosis, xanthomas (skin/tendons), xanthelasma (eye).
Autosomal dominant disease. Feature can include sternum defects, laxity of joints, archacnodactyly, kyphoscoliosis, mitral valve prolapse, dissection aneurysm.
Autosomal dominant disease, characterized by collagen disorder. Other features: hyperelastic, fragile skin. Laxity of joints, mitral valve prolapse, aortic aneurysm (IV), increased risk for bleeding (IV), fragile gingiva, Gorlin sign.
Autosomal dominant disease characterized by neurofibromas, caf�-au-lait spots, enlarged fungiform papilla, lisch nodules, scoliosis, bone cysts, greatly increased risk of leukemia.
Neurofibromatosis type I, von Recklinghausen disease
Autosomal dominant disease characterized by bilateral acoustic neuromas, unilateral acoustic neuromas, neurofibroma or meningioma or glioma or schwannoma, juvenile lens opacity, possible hearing loss.
Neurofibromatosis type II
Autosomal recessive disease characterized by structural defects in hemoglobin. Can have sudden episodes of bone pain, ischemia, infarct; acute chest syndrome, possible storke, blindness, jaw lesions. Treated by hydroxyurea, blood transfusions.
Sickle cell anemia
Autosomal recessive disease, most common lethal AR disease in Caucasians. Affects chloride anion secretion, resulting in thickened mucus, which will cause obstruction or infection in the lungs. Cor pulomale. Pancreatitis, secondary biliary cirrhosis, smal
Autosomal recessive condition. Reduced melanin production, snow white hair, blue irides, red pupils, photophobia, pale pink skin, so increased risk for skin cancer.
Disease characterized by accumulation of glucosylceramide in specific macrophage cells due to a mutation in glucocerebroside production. Primarily affects spleen. 3 types.
Lethal disease characterized by accumulation of gangliosides in the brain. Hypotonia, rapid progressive motor/mental deterioration, seizures, blindness.
Vitamin D resistance disease. X-linked dominant; bowing of long bones. Hypodontia, spontaneous loss of permanent teeth. Extreme bone loss.
Familial hypophosphatemic rickets
X-linked recessive disease causes mental retardation. Sherman paradox. Mitral valve abnormalities, increased joint laxity, enlarged testes, hypotelorism, other physical trademarks.
Fragile X syndrome
Disease characterized by mental retardation, Alzheimer's, heart malformations, simian crease, hyperextensibility of joints, sandal gap, megacolon, risk for leukemia. Characteristic appearances among other things. Caused by nondisjunction.
Down syndrome, trisomy 21
Disease resulting from abnormal sex chromosome number, e.g. XXY. Males have Barr bodies; mildly reduced intelligence; tall/thin, hypogonadism, gynoecomastia, male infertility.
Disease from monosomy (only one X). Hypogonadism, webbed neck, coarctation of aorta, possible dissection aneurysm.
Disease stemming from deletion or inactivation of paternal genes on chromosome 15. Also low IQ, hypotonia, obesity, hypogonadism, small hands and feet.
Disease stemming from deletion or inactivation of maternal genes on chromosome 15. Also severely low IQ, seizures, ataxia, etc.
A hemolytic disorder of a newborn due to Rh incompatibility during a second pregnancy.
The leading cause of death in the first year of life. Sudden death in otherwise healthy infant; no definite etiology.
What are the characteristics associated with acute inflammation?
Abrupt response, short duration, sudden injury, exudative reaction
What are possible outcomes to acute inflammation?
Chronic inflammation, resolution w/ scar, abscess formation, complete resolution
What are the characteristics associated with chronic inflammation?
Persistent injury, proliferative reaction, resolution only when source of injury removed
What are the hallmarks of acute inflammation?
Increased blood flow, increased vascular permeability, recruitment of stimulation of neutrophils, PMNs, platelets, monocytes, macrophages
What are the four cardinal signs of acute inflammation according to Celsus?
Rubor (redness, erythema), tumor (swelling), calor (heat), dolor (pain
What are the systemic signs of acute inflammation due to a severe response?
Fever, leukocytosis, lymphadenopathy
Immediately after an injury, what occurs to the vasculature surrounding it?
Transient vasoconstriction, vasodilation (hyperemia, erythema), leakage of fluid, endothelial cell retraction and gap formation
Why does vascular stasis occur?
As fluid is loss from the vessels, the blood becomes more viscous and flows more slowly; also allows for leukocyte margination, extravasation (diapedesis)
Swelling caused by the leakage of fluid from the bloodstream into the surrounding tissues is known as ?
An exudate that accompanies mild inflammation, is thin, clear, and watery in appearance, and contains mainly plasma fluid with low protein and few cells would be a ______ exudate.
A _______ exudate typically exhibits thick, opaque, white or yellow pus, rich in neutrophils and cell debris, containing plasma fluids and protein. Often accompanies pyogenic bacterial infections.
What are some of the benefits of an inflammatory edema, an increase in vascular permeability and exudation of fluid and plasma proteins?
Dilutes toxins, inactivates toxins, provides nutrients for inflammatory cells, presents antibodies and complement proteins, contains fibrinogen
Movement towards a chemical gradient (directs movement of WBCs to injury)
Characteristics of neutrophils?
60-70% of WBC population; hallmark cell in acute inflammation; phagocytes, short life span, multi-lobular nucleus, granular cytoplasm with lysozymes
Which type of cell accounts for 3-8% of WBCs, follows PMNs as the second line of response to injury during acute inflammation?
Monocytes (large, mononuclear cells, phagocytosis, destroy foreign material with lysozymes)
What is the most important vasoactive mediators that will induce vasodilation, and therefore edema, after injury?
Characteristics of acute inflammation?
Short duration; mostly vascular changes, edema; neutrophils predominant
Characteristics of chronic inflammation?
Longer duration; lymphocytes, macrophages/monocytes present; tissue destruction, attempted tissue repair via angiogenesis and fibrosis/scarring
What are the signs and symptoms of inflammation?
Hyperemia: increased blood flow
Exudate: inflammatory fluid formed as reaction to injury (can be serous or purulent; can be drained either fistula or incision)
Which exudate is mainly plasma fluid and proteins, contains few WBCs, contains complement, etc. inflammatory proteins?
Which exudate contains tissue debris, many WBCs, plasma fluids, and proteins?
Vasoactive factors lead to ___________ and consequently ________. Examples include...?
Increased vascular permeability; edema; histamine, serotonin, bradykinin, LTs/PGs, PAF
The role of chemotactic factors is to __________, resulting in __________. Examples include...?
Recruit inflammatory cells; inflammation; C5a, LTB, formylated peptides, lymphokines, monokines
What are the cellular events in acute inflammation?
Adhesion, or pavementing
Chemotaxis and emigration
Phagocytosis and intracellular degradation
Extracellular release of leukocyte products
Which type of white blood cell has multi-lobed nuclei and is found predominantly in pus?
Cytokines are specific and are produced and released by inflammatory cells, resulting in reduced inflammation and systemic effects like fever. True or false?
False (result in FURTHER inflammation)
What are the effects of prostaglandins in acute inflammation?
Further inflammation, pain (where aspirin works)
Histamine is premade by mast cells and stored in granules to be released upon activation. True or false?
What are the effects of histamine in acute inflammation?
Vasodilation, increased vascular permeability (antihistamine target)
What are the three main free-floating chemical mediators of acute inflammation?
Complement, kinins, and clotting factors
Results of complement in acute inflammation?
Part of the complement cascade; results in increased vascular permeability, attracts inflammatory cells, attacks microorganisms
Effects of kinins in acute inflammation?
Increase vascular permeability, involved in pain
What are possible reasons for chronic inflammation?
Persistent infections by certain microorganisms (tuberculosis, syphilis, some fungi), prolonged exposure to toxic agents, autoimmune diseases
What are the 4 main chronic inflammatory cells and what are their roles?
1. Tissue macrophages - migrate to tissue 24-48 hours later; ingest debris, microorganisms; produce cytokines, inflammatory mediators to activate T-lymphocytes
2. T-lymphocytes - stimulate macrophage activity w/ cytokines
3. Plasma cells (or what B-lympho
How do chemokines, such as RANTES, MCP-1, and MIP-1, recruit monocytes?
Cause changes in integrin configuration for binding to VCAMs, ICAMs for migration to injury
What are some ways that a macrophage (or monocyte) can be activated?
Activated T-cell's lymphokines (e.g. IFN-y), bacterial products (LPS), immune complexes, toxins, physical injury, other cytokines
An activated macrophage will release various factors that affect fibrosis, tissue injury, and have other important actions. What will the release of factors like GFs [PDGF, FGF, TGF-b], fibrogenic cytokines, and collagenases affect?
Fibrosis; angiogenesis; tissue remodeling
An activated macrophage will release various factors that affect fibrosis, tissue injury, and have other important actions. What will the release of IL-1 and TNF-a cause?
Activation of more T cells, acute phase reaction (fever due to PGE, more sleep, lower appetite, muscle wasting, acute phase proteins, hemodynamic effects/shock, neutrophilia), endothelial effects (leukocyte adhesion, more PGI and PAF, pro-coagulant activi
An activated macrophage will release various factors that affect fibrosis, tissue injury, and have other important actions. What are the effects of toxic oxygen metabolites, proteases, neutrophil chemotactic factors, coagulation factors, A.A. metabolites,
Systemic manifestations of chronic inflammation include?
Fever, leukocytosis, acute phase response (increased erythrocyte sedimentation rate [ESR])
In non-specific inflammation, what happens?
Mononuclear cells infiltrate w/ a proliferation of fibroblasts and new blood vessels; initial response to viral infections, parasitic infections, autoimmune disease, malignancy
What characterizes granulomatous inflammation?
Granulomas (collections of activated macrophages = 'epithelioid cells' surrounded by rim of lymphocytes, +/- giant cells)
How do the granulomas of granulomatous inflammation form?
IFN-y and IL-4 released by T lymphocytes can sometimes modify macrophages so that they fuse together to form multinucleated giant cells
Distinguish between the different appearances of granulomas. Epithelioid cells, caseating granulomas, Langhans type giant cells, foreign body type giant cells.
Epithelioid cells - cytoplasm resembles squamous epithelial; long, stringy nuclei
Caseating - epithelioid cells surround central area of necrosis
Langhans - nuclei around periphery, mostly pink epithelioid macrophages
Foreign body - nuclei are scattered h
Cheilitis granulomatosa Melkersson-Rosenthal syndrome are examples of what?
Orofacial granulomatosis, a non-specific granulomatous inflammation affecting the orofacial tissues w/ an unknown etiology
List and define the four methods that a cell will use to adapt in response to a physiological stress.
Atrophy - ?size, ~same number
Hypertrophy - ?size, same number
Hyperplasia - ?tissue size, ? number
Metaplasia - change from one normal, mature cell type to another
Regeneration by same type parenchyma cells is the mitotic capability of a cell population, and/or the capacity of immature precursor cells to divide and differentiate, which will determine the eventual outcome of tissue destruction. Regeneration is the so
The first statement is true; the second statement is false (regeneration and replacement with a scar are the two processes involved in tissue repair)
Regeneration involves three types of cells: labile, stable, and permanent. Match them with their definitions and examples.
a. Terminally differentiated, have lost all capacity for regeneration.
b. Epidermis, mucosa of GI
c. Cardiac myocytes, cell of the l
Labile cells - B, D, G; comprise tissues that are in a constant state of renewal; e.g. epidermis, mucosa of GI, respiratory, urinary, and genital tracts, bone marrow, lymphoid organs
Stable cells - E, F, H; form tissues that normally are renewed very slow
The ability of a stable cell to regenerate depends on the number of steady-state mitoses, not the potential to replicate. True or false?
False (the ability of a stable cell to regenerate depends on the potential to replicate, not the actual number of steady state mitoses)
What is the role of the tissue repair growth factor EGF?
Mitogenic for epithelial cells and fibroblasts
Can you name the 6 tissue repair growth factors expounded upon in lecture?
EGF, PDGF, FGF, TGF-b, VEGF, cytokines (IL-1, TNFa)
What is the role of the tissue repair growth factor PDGF?
Released from platelets as granules, also produced by activated macrophages, endothelial cells, smooth muscle cells, and variety of transformed cells
Induces fibroblast, smooth muscle cell, monocyte migration and proliferation
What is the role of the tissue repair growth factor FGF?
Made by active macrophages, binds to heparin and other anionic ECM components, strong affinity for basement membrane, strongly promotes angiogenesis
What is the role of the tissue repair growth factor TGF-b?
Made by cells in an inactive form that must be cleaved; variety of effects: generally growth inhibitory for epithelial cells, promotes fibrinogenesis and scarring, stimulates fibroblast chemotaxis, production of collagen and fibronectin, inhibits digestio
What is the role of the tissue repair growth factor VEGF?
Many isoforms, but made by tumor cells, promotes angiogenesis and vascular permeability
What is the role of the tissue repair growth factors IL-1, TNFa, both of which are cytokines?
They act as chemotactic and mitogenic factors for fibroblasts, induce synthesis of collagen and collagenases
The basement membrane is required for the orderly renewal of tissue, particularly epithelium. True or false?
Collagen mainly functions to provide mechanical strength and support to the tissues of the body. List the types and were they are dominantly found.
I - bone, skin, tendons, mature scars
II - cartilage
III - embryonic tissues, blood vessels, uterus, GI tract
IV - exclusively in basement membranes
V-XXII - basement membranes
Glycoproteins link ECM components to cells and to one another. This includes _____________ , the most abundant protein in the basement membrane; ____________, which binds integrins; and thrombospondins.
With damage to both the parenchyma and stroma, repair cannot be accomplished by regeneration alone, thus requiring fibrosis. What are the steps of scar formation?
1) Angiogenesis - new, leaky vessels edematous, extravasated RBCs in scar tissue; BM, ECM degradation and remodeling
2) Migration, proliferation of fibroblasts
3) Deposition of ECM, first proteoglycans dominant, then collagen dominant
4) Maturation and o
What are the overall events of wound healing? *could ask a more detailed question but I didn't even read the block of text so
Induction of acute inflammation following injury, parenchyma cell regeneration if possible, migration and proliferation of parenchyma and connective tissue cells, synthesis of ECM components, remodeling of parenchyma and ECM to restore function and increa
What are the three healings by intention?
Primary - clean incision w/ approximated ends; epithelial regeneration predominates over fibrosis; little granulation tissue, less scar tissue
Secondary - cell, tissue loss is extensive; possible extensive granulation tissue, scarring, wound contraction
Factors that can influence wound healing?
Local factors: Wound type, size and location, Vascular supply, Infection, Movement
Systemic factors: Circulatory status, Infection, Metabolic status, Malnutrition
Complications of wound healing: Deficient scar formation: dehiscence and incisional, hernias
What kind of cell receptors are used in innate immunity?
Toll-like, NOD-like, inflammasome, C-type lectin receptors
Humoral immunity targets (intracell, extracell) pathogens.
Cellular immunity targets (intracell, extracell) pathegens.
What are the 2 types of lymphoid tissues?
Generative & Peripheral Lymphoid Organs
What is the function of lymphoid organs?
They are the site of lymphocyte progenitor stem cell development
B cells develop in the ______ and mature in the ______.
Bone marrow, bone marrow
T cells develop in the ______ and mature in the ______.
Bone marrow, thymus
What is the function of peripheral lymphoid organs?
They concentrate antigens, APCs, and B/T lymphocytes for adaptive immune responses - act as a filter
What are some peripheral lymphoid organs?
Lymph Nodes, Spleen, Skin, Mucosa
What is the name of the oral lymphoid tissues?
What are 2 accessory oral lymphoid tissues
Tonsillar arch & the ventral tongue
CD4 T-cells bind Class ___ MHC receptors.
CD8 T-cells bind Class ___ MHC receptors.
What is another name for MHCs?
Human Leukocyte Antigen (HLA) Complex
Which chromosome is responsible for the production of MHC peptides?
Which immune cell secretes cytokines?
What are 4 types of Cytokines?
Which T-cell subtype is used as an indicator of immune health, and what is the range for a normal functioning immune system?
Normal Range: 500-1500
When B cells are stimulated, what do they turn into?
T/F: B-lymphocytes, when stimulated, travel to the site of infection and release antibodies there.
FALSE: B-lymphocytes do NOT need to migrate to the site of infection. Instead, they release antibodies into the blood/lymph which are then transported to the tissues
Where are Natural Killer Cells produced?
In the thymus and bone marrow
What are the precursor cells of NK cells?
Where do APCs go to present themselves to T-lymphocytes?
The lymph nodes
What is the name of dendritic cells in the epithelium?
Besides DC cells, what are 2 other APCs?
Macrophages and B cells
CD4+ subtype TH1
-defense against intracellular pathogens
-autoimmunity, chronic inflammation
CD4+ subtype TH2
-stimulates B cells eosinophils
-releases IgE in response to allergic reactions
-defense against helminths
IL-4, -5, -13
CD4+ subtype TH17
-defense against extracellular pathogens
What is hypersensitivity?
It is an immune response that leads to tissue injury & disease (sometimes used synonymously with allergy)
Of the 4 classes of hypersensitivity, which ones are antibody mediated, and which ones are cell mediated?
Antibody Mediated: Types 1-3
Cell Mediated: Type 4
What is Type I Hypersensitivity?
Immediate-type & Anaphylaxis
What is Type II Hypersensitivity?
What is Type III Hypersensitivity?
Immune Complex-mediated Disease
What is Type IV Hypersensitivity?
Describe the initial event of Type I Hypersensitivity.
APCs engulf antigens
TH2 cells activated B cells --> plasma cells
IgE binds mast cells & basophils on the Fc receptors
Mast/basophil cells remain primed for years
What happens when an antigen is recognized a second time?
Antigen bind IgE
IgE cross-link activates mast cells/basophils
Within minutes, other mediators (degranulation) are released into the tissue & bloodstream
Results in a local OR systemic reaction
What are the 4 classifications of allergens?
Inhalants, Ingestants, Injectants, Contactants
What do cytokines do?
-recruit & activate leukocytes
-mediate inflammation and sometimes promote tissue destruction
What are histamines effects on smooth muscle contraction, mucus secretion, & blood vessels?
Increase all of them (vasodilate)
How does prostaglandin affect blood vessels, painsensitivity, and the bronchioles?
Increases vasodilation/permeability, increases sensitivity to pain, and constricts the bronchioles
What do Leukotrienes do to the muscle and blood vessels?
Increases smooth muscle contraction and increases vascular permeability
What are the 2 Type I Hypersensitivity reactions?
Atopy & Anaphylaxis
What is the big difference between Atopy & Anaphylaxis?
Atopy is local and Anaphylaxis is systemic
How does the respiratory system react to Type I mediators?
How does the digestive tract react to Type I mediators?
How does the skin react to Type I mediators?
-urticaria (hives), pruritis (itching), redness
How does the cardiovascular system react to mediators?
What are 2 kinds of hives (urticaria)?
Wheal - a swollen area of the skin
Flare - redness of the skin
Swelling of the face around the eyes, lips, tongue, uvula, and hands
Describe the sequence of events of anaphylactic shock.
Bronchioles contract and compromise the airways dyspnea arteriole dilation leads to a drop in blood pressure causes circulatory collapse -SHOCK
How can you treat anaphylactic shock
Can you name some medication cousins?
What are some symptoms of a local anesthetic allergic reaction?
How can you diagnose an allergy?
-serologic testing of IgE
-intradermal - you inject a diluted allergen
-patch testing - surface contact
What is the function of Corticosteroids?
They prevent the plasma cells from synthesizing IgE & inhibit T cell
What is the function of Xolair?
It inactivates IgE
What is the function of Nalcrom/Cromolyn?
It prevents degranulation on the surface of mast cells
What do antihistamines, aspirin, epinephrine, etc do?
They counteract the effects of cytokines on different targets
-it is for severe allergies
-it consists of multiple injections (3-5 days apart) of increasing concentrations of allergen
-continues for 3 years or longer
What are the 2 main antibodies involved in Type II Hypersensitivity?
What 3 mechanisms are responsible for Type II effects?
Antibody-mediated Cellular Dysfunction
Examples of Opsonization reactions include which of the following:
-transfusion reactions (blood)
-Autoimmune hemolytic anemia
Transfusion reactions, rhesus disease, autoimmune hemolytic anemia
In Transfusion reactions, which antibody is responsible for activating the complement that lyses RBCs?
Blood type A can receive blood from _______
A & O
Blood type B can receive blood from _______
B & O
AB is a universal _________ and O is the universal _______
AB - universal recipient
O - universal donor - can only receive type O blood
What are some examples of Antibody-mediated cellular dysfunction diseases?
-Graves disease (hyperthyroidism)
-Acute rheumatic fever
Which antibodies are involved in Type III Hypersensitivity and what does it do to form an immune complex?
IgG, IgM, sometimes IgA
-they bind to circulating antigens to form an immune complex that may become implanted onto basement membranes
What do the immune complexes do that cause disease?
They activate the complement which leads to the recruitment of PMNs and monocytes, initiating phagocytosis and tissue damage
There are 3 stages of immune complex-mediated disease. In which stage does tissue injury such as arthritis and vasculitis occur?
In which stage are PMNs and monocytes activated?
How early does Phase 1 begin?
Within 1 week
List some examples of immune complex-mediated disease.
T/F: Type IV Hypersensitivity involves both T & B lymphocytes.
FALSE: only T lymphocytes
What is another name for Type IV Hypersensitivity? (hint: it has to do with time)
Delayed antigenic reaction (24-48 hrs)
What is the name of the test used to diagnose TB?
What category could poison ivy, cinnamon, and dental amalgam be put under in terms of Type IV reactions?
If a patient's body is rejecting/reacting to amalgam, what kind of lesion forms on the buccal mucosa?
A lichenoid lesion
What are some features of cinnamon-related oral lesions?
-angular cheilitis (the fissures at the corner of the mouth)
Lymphocytes are infection-fighting WBCs and constitute 25% of WBCs
What percentage of lymphocytes are T cells, B cells, and NK cells?
T cells: 80%
B cells: 10%
NK cells: 10%
Vaccinations expose a person's immune system to _______ forms of bacteria.
How many species of Influenza are there?
Which influenza viruses cause the yearly flu?
Influenza A and B
When scientists gather to make the next year's flu vaccine, how many strains are they aiming to prevent?
3 or 4
Which influenza virus is generally more virulent?
Why is vaccination against H3 strains less effective than other strains?
H3 strains mutate faster as they move through the population
What are the 2 types of errors that can be made by the immune system?
Fail to detect invading orgs. infection
Fail to recognize self cells autoimmune