Infection, Immunity, & Inflammation: Immune Response Flashcards
these unique proteins are found on the surface of all body cells of that person and serve as a “universal product code” or a “cellular fingerprint” for that person. capable of stimulating immune response
signify self or non-self; important for transplants
human leukocyte antigens (HLAs)
these cells come from stem cells and mature in bone marrow; nonspecific ingestion and phagocystosis of microorganisms and foreign protein; inflammation response
neutrophil
- short life span (12-18hours)
- small - only undergo one episode of phagocytosis each
- continuous, instant, nonspecific protection
- used to measure a pts risk for infection
segmented neutrophils
- 62% of total WBC
- more is good, means more resistance to infection
- should not be many in blood
- a lot of these a.k.a. Left shift = sepsis
- less mature neutrophils
band neutrophils
- 5% of total WBC
- “bands”
neutrophils in the blood change from being mostly segs (mature) to mostly bands, less mature neutrophil
indicates pts bone marrow cannot produce enough mature neutrophils to keep pace with the continuing incfection and is releasing immature neuts
Left Shift (bandemia)
refers to proximitiy of bands on the neutrophil pathway (further left than segs)
- part of inflammation
- destruction of bacteria and cellular debris
- move from blood into tissue where they form macrophages
monocyte
- 3% of total WBC
- important in immediate inflammatory responses
- stimulate longer-lasting immune responses of AMI and CMI
- large size makes them very effective at taking a part in many phagocytic events
- found in tissues (liver, spleen, intestinal tract)
macrophages
- (monos = 3% of total WBC)
- release heparin, histamine, serotonin, kinins, and leukrtrienes into blood
- heparin - inhibits blood and protein clotting
- histamine - constricts small veins prevents venous return
- kinins - dilate arterioles increase capillary permeability
- causes blood plasma to leak into interstitial space (vascular leak syndrome)
basophils
- 0.5% of total WBC
- active against infestations of parasitic larvae
- limits inflammatory reactions
- increase during allergic response
Eosinophils
- 1.5% of total WBC
the engulfing and destruction of invaiders, rids the body of debris after tissue injury
phagocytosis
Phagocytosis process:
- Exposure and invasion of organisms
- Attraction (chemotaxins attract neuts and macrophages)
- Adherence (opsonins)
- Recognition (examination of HLAs)
- Cellular Ingestion
- Phagosome formation (attack of ingested particle)
- Degradation (brake down engulfed target)
Sequence of Inflammatory Responses:
(always nonspecific)
-
vascular - injured tissues and basophils release chemicals to bring blood to area, macrophage secrete cytokine (release more WBC, increase release of neuts
- redness and edema usually subside within 72h
- cellular - neutrophils stage, phagocytosis of organisms and dead tissue, lasts for a few days but if longer the bone marrow will start releasing bands
- repair and replacement - begins at time of injury just finishes last, WBC trigger healthy cells to divide, new blood vessel growth, scar tissue formation
becomes sensitized to specific foreign cells and proteins and produce antibodies directed specifically against that protein; stimulated by macrophage that is developed in thymus and pericorical areas of lymph nodes
(part of AMI)
B-lymphocyte
Sequence of the seven steps required to timulate antibody-mediated immunity:
- exposure or invasion
- antigen recognition (w/ macrophage & CD4 tcell-helper)
- sensitization (sensitized bcell divides into plasma cell and memory cell)
- antibody production and release
- antibody-antigen binding
- antibody-binding actions
- sustained immunity (memory)
produces antibodies against the senitizing antigen; developed from sensitized B-lymphocyte(cell)
plasma cell
a sensitized B-cell but does not start to function until the next exposure of the same antigen
memory cell
a clumping action that results from the antibody linking antigens together, forming large and small immune complexes; slows the movement of the antigen in body fluids; irregular shape of the antigen-antibody complex allows that complex to be attacked more easily by macrophages and neutrophils
Agglutination
cell membrane destruction, antibody binding to membrane-bound antigens of some invaders
Lysis
actions triggered IgM & IgG (antibodies) that can remove or destroy antigen; beginning of cascade
complement activation and fixation
antibody molecules bind so much antigen that large antigen-antibody complexes are formed (too heavy to stay in blood); forms large precipitate and is phagocytized by neuts and macrophages; similar to agglutination but larger response
precipitation
process by which a pathogen is marked for ingestion and destruction by phagocytosis (activated complement compounds {IgM, IgG}, dead neuts, antibodies)
perfume to attract macrophages and neuts
opsonization
w/ opsonins (part of adherence)
- first antibody formed by a newly sensitized B-lymphocyte plasma cell
- 10-15% of circulating antibody population
- part of agglutination and precipitation
- LARGE (five antibody group) with 10 potential binding sites
- activator of complement pathway
IgM
- composes at least 75% of ciculating antibody population
- important for second and subsequent exposures to antigens
- sustained long-term immunity
- activates complement pathway, enhance phagocytosis
- involved in antibody-dependent cell-mediated non-self cell killing action of natural killer cells
IgG
the immunity that a person’s body learns to make (or can receive) as an adaptive response to invasion by organisms or foreign proteins
adaptive immunity
when antigens enter the body and the body responds by making specific antibodies against the antigen
Natural (eg. chickenpox)
Atrificial (eg. vaccination & immunization)
active immunity
occurs when antibodies against an antigen are in a person’s body but were not created there; short term protection against a specific antigen
Natural (mother to fetus cia placenta)
Artificial (used when a person is exposed to a serious disease which they have little to no immunity to)
Passive Immunity
Process of Cell-Mediated Immunity:
- CD4+ t-cell (helper/inducer)
- CD8+ cells (suppressor)
- Cytoxic/cytolytic T-cells
- CD16+cellsNatural Killer Cells
enhances immune activity through secretion of various factors, cytokines, and lymphokines; becomes sensitive by macrophage
CD4+ tcell (helper/inducer)
- *selectively** attacks and destroys non-self cells, including virally infected cells, grafts, and transplanted organs; suppressor cell subsets; destroy human cells that contain a processed antigen’s HLAs
- likes to go for cells infected by parasites, viruses, or protozoa-
Cytotoxic/cyctolytic T-cells (Tc-cells)
have direct cytoxic effect on some non-self cells without first being sensitized. “Seek and Destroy”
-likes to go for cancer cells and virally infected body cells-
Natural Killer (NK) cells
small protein hormones produced by many WBCs; act like “messengers” that tell specific cells how and when to respond
Cytokines
(monokines - if created by macrophages, neutrophils, eosinophils, and monocytes)
(lymphokines - if created by T-cells)
Patients at greatest risk for hyperacute rejection:
- those receiving from ABO blood type different from their own
- have receivedmultiple blood transfusions at any time in life
- history of multiple pregnancies
- have received a previous transplant
What cell types must be suppressed to prevent acute rejection of transplanted organs?
- Natural Killer cells NK
- Cytoxic/cytolytic T-cells
- Antibody-mediated response (only)
- triggers blood clotting cascade, occludes vessels and leads to ischemic stroke
- rejection cannot be stopped
- immediate! host’s blood has pre-existing antibodies to one or more of the antigens present in the donated organ
- treat by immediate removal of organ
Hyperacute rejection
- occurs within 1week-3months
- does not mean loss of transplant
- leads to organ destruction via necrosis
- includes both AMI and CMI
- treat with immunosuppressants
Acute graph rejection
- similar to chronic inflammation and scarring
- results in reduced function
- long standing
- major cause of death in heart transplant clients
- fibrotic and scar like tissue is formed
- accelerated graft atherosclerosis
- more than 3months after transplant
chronic rejection
hardening of the arteries, a common disorder that occurs when fat, cholesterol, and other substances build up in the walls of arteries and form hard structures called plaques. Over time, these plaques can block the arteries and cause problems throughout the body.
atherosclerosis
management of transplant rejection:
- continuous immunosuppression
- cyclosporine
- prednisolone
- Tacrolimus(Prograf)
- sirolimus (Rapamune)
- everolimus (Certican)
- infection prevention (due to immunosuppre)
Elevated if there is a non self bacteria in system
neutrophils (62%)
Elevated if there is a non self virus in system
monocyte (macrophage) 3%
Elevated if there is a non self parasite in system
eosinophils (1.5%0
