0 Bewertungen0% fanden dieses Dokument nützlich (0 Abstimmungen)
30 Ansichten6 Seiten
Immune System cells constantly come in contact with other body cells. Immune cells compare the HLAs to determine if the cell is "self" or "non-self" immune function is most efficient when people are in their 20s and 30s.
Immune System cells constantly come in contact with other body cells. Immune cells compare the HLAs to determine if the cell is "self" or "non-self" immune function is most efficient when people are in their 20s and 30s.
Copyright:
Attribution Non-Commercial (BY-NC)
Verfügbare Formate
Als DOC, PDF, TXT herunterladen oder online auf Scribd lesen
Immune System cells constantly come in contact with other body cells. Immune cells compare the HLAs to determine if the cell is "self" or "non-self" immune function is most efficient when people are in their 20s and 30s.
Copyright:
Attribution Non-Commercial (BY-NC)
Verfügbare Formate
Als DOC, PDF, TXT herunterladen oder online auf Scribd lesen
• Overview: Body has some defenses to prevent organisms
from gaining access to the internal environment, such as intact skin and mucous membranes, normal skin flora, and natural chemicals on the skin.
• Purpose of inflammation and immunity: to meet the need
for human protection by neutralizing, eliminating, or destroying.
• HLAs (Human leukocyte antigens
o Present on all body cells
o Unique to each person
o Determine tissue type of a person
o Other names: Human transplantation antigens,
Human histocompatibility antigens, Major histocompatibility antigens, Class I antigens
o Humans have 40 major HLAs
o Antigens present are determined by which MHC gene
alleles were inherited from the parents
o Key for recognition and self-tolerance! : Immune
system cells constantly come in contact with other body cells. The immune cells compare the HLAs to determine if the cell they have come in contact with is “self” or “non-self”. If self, then the body leaves it alone but if the cell is non-self then the body takes action to get rid of it.
• Immune System/function changes during a person’s
lifetime according to the nutritional status, environmental conditions, drugs, disease, age. Immune function is most efficient when people are in their 20s and 30s.
• Organization of the Immune System
o Immune system cells come from the bone marrow.
o Stem cells are pluripotent meaning that each cell has
more than one potential outcome. o Growth factors which are specific chemicals that direct growth and determine what the stem cell will be.
o White blood cells are the immune system cells.
Actions of the White blood cells are: recognition of self, destruction of foreign invaders, cellular debris, and healthy or abnormal self cells, production of antibodies, complement activation, and production of that stimulate increase formation of leukocytes in bone marrow and increase specific leukocyte activity.
o 3 processes that are needed for human protection
o It is a short term but an immediate reaction. It is also
a non-specific defense
o Infection is usually accompanied by inflammation,
however; inflammation can occur without an infection.
o Cell Types involved in inflammation
Neutrophils – 55% to 70% of total white blood
cells. Growth requires 12-14 days. More than 100 billion are released into circulation each day. Life span of 12-18 hours. Take part in phagocytosis but only mature ones. Small energy supply. (ANC: the percentage and number of mature neutrophils in the circulating blood).
Macrophages – Stored in the liver, spleen, and
intestinal tract. They are mature monocytes. They have specific functions such as: phagocytosis, repair, antigen processing, and secretion of cytokines. Long life spans. Can renew energy supplies.
Basophils – 1% of total white blood cells. These
can cause manifestations of inflammation. Contain chemicals: heparin, histamine, serotonin, kinins, and leukotrienes. Vascular leak syndrome (blood plasma to leak into the interstitial space).
Eosinophils – 1-2% of total white blood cells.
Act against parasitic larvae, and can limit the inflammation reactions.
o Phagocytosis
Exposure and invasion – leukocytes must first
be exposed to organisms/foreign bodies
Attraction: occurs only when the white blood
cell comes into contact with the target
Adherence: phagocytic cell first binds to the
surface of the target
Recognition: when it recognizes the target cell
as non-self
Cellular ingestion: when the target cell is
brought into the phagocytic cell (engulfs) and forms a vacuoles
Phagosome formation: granules break and
release enzymes that attack target cell
Degradation: target is broken into smaller
pieces.
o Sequence of Inflammation Response
5 cardinal manifestations of inflammation:
warmth, redness, swelling, pain, and decreased function.
Stage One: Changes in blood vessels,
hyperemia and edema, 24 to 72 hours, and the macrophage is the major cell.
Stage Two: Neutrophilia occurs. Exudate in the
form of pus. Limits the helpful effects of inflammation and increases the risk for sepsis.
Stage Three: Tissue repair and replacement.
White blood cells trigger new blood vessel growth (angiogenesis) and scar tissue formation. • Antibody Mediated Immunity
o Purpose
B cells are to become sensitized to a specific
antigen and produces antibodies against that antigen.
B cells have the most direct role in AMI.
B cells start as stem cells in the bone marrow,
the primary lymphoid tissue. After they migrate into secondary lymph tissues such as the spleen, lymph nodes, tonsils, and mucosa.
o Antigen-Antibody Interactions
Exposure or invasion: the antigen must first
enter the body
Antigen-recognition: recognize the antigen as
“non-self”
Lymphocyte sensitization: B cells recognize the
antigen and is now sensitized to his antigen
Antibody production and release: antibodies
are produced against the antigen and search out the antigen.
Antibody-antigen: y shaped antibodies and the
specific antigen are bound together
Sustained immunity: provides long lasting
immunity to a specific antigen resulted from B cells
o Antibody Classification
IgM – present upon the first exposure to the
antigen
IgG – present upon re-exposure
o Acquiring antibody mediated immunity
Natural active: occurs when antigen enters the
body with out human assistance and the body responds by making antibodies (*Most effective and longest lasting!!).
Artificial active: protection that is developed by
a vaccination or immunization
Natural passive – occurs when antibodies are
passed from the mother to fetus (placenta, breast milk).
Artificial passive – involves injecting a person
with antibodies that were produced in another person.
• Cell Mediated Immunity
o Cell Types Involved in CMI
Helper T cells – Easily recognize self versus
non-self cells. Helpers secrete lymphokines that can enhance the activity of other white blood cells. Increase bone marrow production of stem cells and speed up their maturation.
Suppressor T cells – Prevent hypersensitivity.
Help to inhibit the growth and activation of immune system cells.
Cytotoxic T cells – Destroy the cells by making
holes in the membrane causing it to lyse and die.
Natural killer cells – Most effective in
destroying unhealthy or abnormal self cells.
• Types of Rejection and Treatment
o Hyperacute rejection
Begins immediately
Occurs mostly in transplanted kidneys
Patients at greatest risk are: Those who have
received donated organs of a different ABO type, Have received multiple transfusions, history of multiple pregnancies, and received a previous transplantation.
Process can not be stopped once it has started
and the rejected organ is removed as soon as its diagnosed.
o Acute rejection
Within one week to three months
Necrosis leads to organ’s destruction
Inflammation response and causes lysis of
organ cells.
Does not automatically mean patient will lose
new organ
o Chronic Rejection
No cure
Decreased organ function
o Treatment of Transplant Rejection
Immune suppression: Cyclosporine, Imuran,
Mycophenolate. * Treatment with these causes an increased risk for infections and cancer development
(Current Topics in Microbiology and Immunology 386) Michael B. A. Oldstone, Richard W. Compans (Eds.) - Influenza Pathogenesis and Control - Volume II (2015, Springer International Publishing)