Immune Response & Cytokines Flashcards
Can be cell-mediated (cellular) and antibody-mediated (humoral)
adaptive immunity
Involves B cell activation, production of antibodies in blood plasma and lymph
humoral immunity
About 1 to 2 weeks for a measurable amount of antibody to be observed
lag phase
Rapid increase in the concentration of antibodies observed
exponential phase
Production and degradation of antibodies are balanced
steady state
Immune system begins to shut down
decline phase
Accomplished by phagocytosis. Most injected Ag is
removed within minutes, but complete removal may take months or years
antigen elimination
After exposure to antigen, there is latent pd of
approx. 5 to 15 days before antibody appears in the serum
the primary response
Second or subsequent exposure to the same antigen elicits secondary response. there is rapid antibody response usually within 2 to 4 days after antigen exposure
the secondary response
DURATION:
Long lag phase, short plateau, and rapid decline
primary response
DURATION:
Short lag phase, long plateau, and gradual decline
secondary response
cells in primary response
plasma cells
cells in secondary response
memory cells
type of antibody in primary response
IgM
type of antibody in secondary response
IgG
antibody titer in primary response
low
antibody titer in secondary response
high
antibody affinity in primary response
low
antibody affinity in secondary response
high
antibody avidity in primary response
high (increase valence)
antibody avidity in secondary response
high
Action of T cells; produces cytokines
CELLULAR (CELL-MEDIATED) IMMUNITY
CD4 cells respond to antigen recognition
CD8 cells respond to antigen recognition
CELL-MEDIATED IMMUNE RESPONSE
Antigens that stimulate this response are mainly
intracellular
T CELLS AND CELL MEDIATED IMMUNITY
Requires constant presence of antigen to remain
effective
T CELLS AND CELL MEDIATED IMMUNITY
Unlike humoral immunity, cell mediated immunity is not transferred to the fetus
T CELLS AND CELL MEDIATED IMMUNITY
It is life-threatening systemic inflammatory syndromes involving elevated levels of circulating cytokines and immune-cell hyperactivation that can be triggered by various therapies, pathogens, cancers and autoimmune conditions
cytokine storm
(T/F)
The laboratory findings in cytokine storm are
variable and influenced by the underlying cause.
true
Universally elevated and correlate with severity
C-reactive protein (CRP)
Many patients have hypertriglyceridemia and various blood-count abnormalities, such as leukocytosis, leukopenia, anemia, thrombocytopenia, and elevated ferritin and d-dimer levels
cytokine storm
key cellular component of immunity
T cells
Helper T cells activate B cells to maturity and produce antibody
CD4+
Cytotoxic T cells that directly protect from viral infection by cell lysis
CD8+
Early thymocytes lack CD4 and CD8 markers
double-negative stage
Express both CD4 and CD8 antigens
double-positive stage
The development of two distinct T-cell populations
CD4+ (helper-inducer); CD8+ (suppressor cytotoxic)
mature T cell
The loss of Tdt enzyme
mature T cell
Produce interferon and tumor necrosis factor
Th1 cells
Protect cells against intracellular pathogens
Th1 cells
Responsible for cell-mediated effector mechanism
Th1 cells
Produce a variety of interleukins, IL-4, IL-5,IL-10, and IL-13
Th2 cells
Essential role is to help B cells produce antibody against extracellular pathogens
Th2 cells
Central role in immune response
T HELPER (TH) CELLS
Most are CD4+; CD8-
T helper (TH) cells
Recognize antigen on the surface of antigen presenting cells (e.g.: macrophage)
T helper (TH) cells
Activate macrophages
T helper (TH) cells
Stimulate B cell growth and differentiation
T helper (TH) cells
50-60% in the peripheral blood
T helper (TH) cells
produces IL-2, IL-3, GM-CSF, IFN-gamma
T helper (TH) cells
Destroy target cells
cytotoxic T (Tc) cells
Most are CD4 negative (CD4 -),CD8+
cytotoxic T (Tc) cells