Exam 2- Alterations In Immunity And Inflammation Flashcards
Type I hypersensitivity reactions
Type I reactions are mediated by antigen-specific IgE and the products of tissue mast cells. Most common allergies (e.g., pollen allergies) are type I reactions. In addition, most type I reactions occur against environmental antigens and are therefore allergic.
Ex: anaphylaxis to bees (IgE-mediated)
Autoimmunity
Self-antigens are usually in a state of tolerance, or immunologic homeostasis, with the host’s own immune system. Central tolerance develops in humans during the embryonic period as autoreactive lymphocytes are either eliminated or suppressed in the primary lymphoid organs during differentiation and proliferation of immature lymphocytes. Clones of cells with antigen receptors for self-antigens are deleted. Peripheral tolerance is maintained in the secondary lymphoid organs through the action of T-regulatory lymphocytes or antigen-presenting dendritic cells. Autoimmunity is a breakdown of tolerance in which the body’s immune system begins to recognize self-antigens as foreign. In most autoimmune conditions the mechanism of tolerance breakdown is unknown, although several potential mechanisms have been suggested.
Alloimmunity
Alloimmunity occurs when an individual’s immune system reacts against antigens on the tissues of other members of the same species. The two clinically relevant examples of this reactivity are (1) several transient neonatal diseases (in which the maternal immune system becomes sensitized against antigens expressed by the fetus) and (2) transplant rejection and transfusion reactions (in which the immune system of a recipient of an organ transplant or blood transfusion reacts against antigens on the donor cells). Ex: Alloimmune neutropenia—in which maternal antibody against neutrophils destroys neutrophils in the neonate.
Systemic lupus erythematosus (SLE)
chronic, multisystem, inflammatory disease and is one of the most common, complex, and serious of the autoimmune disorders. 24 SLE is characterized by the production of a large variety of autoantibodies against nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and many other self-components. The most characteristic autoantibodies produced in SLE are against nucleic acids (e.g., single-stranded deoxyribonucleic acid [DNA], double-stranded DNA), histones, ribonucleoproteins, and other nuclear materials. it is most common in women. Clinical manifestations of SLE include arthralgias or arthritis (90% of individuals), vasculitis and rash (70% to 80% of individuals), renal disease (40% to 50% of individuals), hematologic abnormalities (50% of individuals, with anemia being the most common complication), and cardiovascular diseases(30% to 50% of individuals). As with most autoimmune diseases, the disease process develops slowly (up to 10 years from occurrence of the first autoantibody until diagnosis) 25 and is characterized by frequent remissions and exacerbations. Because the signs and symptoms affect almost every body system and tend to be intermittent, SLE is extremely difficult to diagnose. This has led to the development of a list of 11 common clinical findings. The serial or simultaneous presence of at least four of them indicates that the individual has SLE 26 :
Facial rash confined to the cheeks (malar rash)
Discoid rash (raised patches, scaling)
Photosensitivity (skin rash developed as a result of exposure to sunlight)
Oral or nasopharyngeal ulcers
Nonerosive arthritis of at least two peripheral joints
Serositis (pleurisy, pericarditis)
Renal disorder (proteinuria of 0.5 g/day or cellular casts)
Neurologic disorders (seizures or psychosis)
Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia)
Immunologic disorders (positive lupus erythematosus [LE] cell preparation, anti–double-stranded DNA, anti-Smith [Sm] antigen, false-positive serologic test for syphilis, or antiphospholipid antibodies [anticardiolipin antibody or lupus anticoagulant])
Presence of antinuclear antibody (ANA)
ABO system
consists of two major carbohydrate antigens, labeled A and B. These two carbohydrate antigens are codominant, which means that both A and B can be simultaneously expressed, resulting in an individual having any one of four different blood types. The erythrocytes of persons with blood type A have the type A carbohydrate antigen (i.e., carry the A antigen), those with blood type B carry the B antigen, those with blood type AB carry both A and B antigens, and those of blood type O carry neither the A nor the B antigen. A person with type A blood also has circulating antibodies to the B carbohydrate antigen. If this person receives blood containing B antigens (i.e., blood from a type AB or B individual), a severe transfusion reaction occurs and the transfused erythrocytes are destroyed by agglutination or complement-mediated lysis. Similarly, a type B individual (whose blood contains anti-A antibodies) cannot receive blood from a type A or AB donor. Type O individuals, who have neither A nor B antigen but have both anti-A and anti-B antibodies, cannot accept blood from any of the other three types. These naturally occurring antibodies, called isohemagglutinins, are immunoglobulins of the IgM class and are induced by similar antigens expressed on naturally occurring bacteria in the intestinal tract. Because individuals with type O blood lack both types of antigens, they are considered universal donors, meaning that anyone can accept their red blood cells. Similarly, type AB individuals are considered universal recipients because they lack both anti-A and anti-B antibodies and can be transfused with any ABO blood type.
Immunologic homeostasis
Steady state of tolerance to self-antigens or lack of immune reaction against environmental antigens.
Alloimmunity
Immune system of one individual produces an immunologic reaction to tissues of another individual.
Ex: blood reaction
Hypersensitivity
Altered immunologic response to an antigen that results in disease or damage to the host.
Requires sensitivity against a particular antigen that results in primary and secondary immune responses
Allergy
Deleterious effects of hypersensitivity to environmental antigens.
Sensitized
When an adequate amount of antibodies or T cells is available to cause a noticeable reaction on re-exposure to the antigen
Delayed hypersensitivity reactions
Involve T lymphocytes but not B lymphocytes
Antibody dependent cell mediated cytotoxicity
Target cells die by apoptosis
Autoimmunity
Occurs when the immune system reacts against self antigens to such a degree that the person’s own tissues are damaged but antibodies or autoreactive T cells
Defective peripheral tolerance is a factor
Type O blood
Considered universal donor’s because the red blood cells lack A and B antigens
Type II hypersensitivity reaction
Involve antigens only expressed in specific tissues.
Ex: hemolysis after mismatched blood transfusion, Graves dz
