Immune System Flashcards
Immunity types
Innate
Resistance
Adaptive
Barriers to infection
Skin
Mucosal membranes
Innate immunity
Nonspecific resistance
Genetically encoded to recognize:
-Foreign substances (non-self)
-Common pathogenic features
Adaptive immunity specific resistance involves
Lymphocytes
Antibodies specific to the pathogen (B-cells)
Innate immune cells
Produced in bone marrow and circulate in the bloodstream:
Phagocytic cells
Neutrophils-monocyte-macrophages
Phagocytic cells
Engulf and kill microbes
Attachment
Ingestion
Digestion
Egestion
Inflammation
Thorn enters
Pulls cells to help protect
Phagocytosis of bacteria
RBC and other cells and fibers cause abcess
Inflammation function
Rapid
Consistent
Systemic activation can result in septic shock
Chronic inflammation can lead to tissue damage (RA)
Fever
Inhibit microbial growth
Encourage tissue growth
Heightening phagocytosis
Pyrogens
Affect hypothalamus
Elevating body temp
Fragments from pathogens
Cytokines produced by leukocytes
If temp rises above 105 can cause convulsions and death
Cytokines
Chemical messengers involved in innate immunity:
Inflammation
-recruits cells
-increases vascular permeability
Fever
-pyrogens
The complement system
Targets pathogens for destruction
Sequential activations of circulating plasma proteins
Resistance to viruses
Interferons
Natural killer cells
Interferons
Cytokines with antiviral activity
Natural killer cells
Recognize and kill
Tumor cells
Virus-infected cells
Innate immune response recap
-Rapid
-Not pathogen-specific (same response for all pathogens)
-consistent
-macrophages, neutophils, natural killer cells
-complement=bring more cells and put holes in pathogens membrane
-cytokines, interferons
-inflammation, fever
-septic shock
Adaptive immune response
Takes time to develop
Specific (different response based on pathogen)
Efficacy improves with time (due to its memory)
Properties of adaptive immunity
Specificity (recognition of molecular structures)
Self-tolerance
Minimal damage to self
Memory
B cells
Produce antibody molecules
-proteins
-binds to antigenic determinants
-neutralize toxins
-block infections
-opsonize pathogen (makes them eaiser to eat)
-humoral response
Hellper T cells
-participate in B cell maturation
-Regulate inflammatory response
Lymphocytes
Produced in bone marrow
Mature in Primary lymphoid tissues:
T cells mature in THYMUS
B cells mature in BONE MARROW
Mature lymphocytes circulate in secondary lymphoid tissue until they encounter an antigen they recognize
How lymphocytes work
Use cell-surface receptors to detect non-self (antigens)
Each have an antigen receptor
Recpetor specificity
Created during development
Somatic gene recombination:
cell puts together molecule to create own antigen receptor
Clonal selection
- B cells binds antigen
- T cell activates B cell
- proliferation: create more cells
- differentiation: can turn into plasma or memory cells
Clonal selection contribution
Contributes to both immune function and control
Humoral immunity
Results in secretion of immunoglobulin molecules or antibody
Antibody is produced by B cells with help from T cells
IgM
The first to appear in circulation after B cell stimulation (too big to get out of bloodstream and short-lived)
IgG
(Gamma globulin)
The major circulating antibody
Provides immunity to the fetus and newborn
IgA
Provides resistance in the resp and GI tract
*found in colostrum (first milk mom produce after birth)
IgE
Role in allergic reactions
IgD
A cell surface receptor on B cells
Viral inhibition
Antibody bind to viral surface to prevent viral attachment to other cells
Neutralization
Antibodies called antitoxins combine and neutralize toxins and prevent them from attaching
Opsonization
Antibodies called opsonins coat baterical cells
Prevents them from attaching
How memory cells work
Primary antibody response IgG is high and so is Igm
Secondary IgG increases and its faster response because of antibodies and memory. Igm decrease.
Difference in B and T cells recognizing antigens
B: recognize native protein antigens and bind to intact molecules
T: recognize degraded fragments of pathogen proteins which result from antigen processing by phagocytic cells
T cell receptor recognizing antigen
- Pathogen is taken apart
- Pathogen proteins are unfolded and cut into small pieces
- Peptides bind to MHC and push it to surface
- T cell bind to peptide
MHC (proteins)
Tissue typing proteins
On cell surface
Processed antigen peptides attach to MHC so T cells can recognize them.
CD8 T cell
Recognize killer cell
Bind to:
MHC class I
CD4 T cell
Recognize helper cell
Bind to:
MHC class II
What happens when immune function fails
Immunodeficiency
Types of immunodeficiency
Congenital
Acquired
Eg.
-HIV infects and kill Cd4 T cells
-Both humoral and cell-mediated immune responses decrease
Autoimmunity
Misdirected immune responses can damage self tissue
Eg. childhood viral infection of URT reaction cause T cells attack and kill pancreatic B cells
Hypersensitivity
Immune reaction to harmless substances may cause hypersensitivity
Eg. inhaling pollen produce symptoms of a resp infection
what do immune response and memory result from?
selection of responsive clones
how do clonal selection contribute to preventing autoimmunity?
Self-reactive clones are selected for deletion during development resulting in self-tolerance
three outcomes of the complement system
Enhanced phagocytosis
Recruitment of phagocytic cells
Membrane lysis
Cytotoxic (killer) t cells
-kill infected cells
-regulatory t cells
-cell mediated immunity
adaptive immune response cells
Lyphocytes
Cytokines
Antibodies
Cytotoxicity
what initiates the complementary system?
Specific antibody
Pathogen cell surface characteristics
