ANSC4650 Midterm: A+ Midterm I Review Guide

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3 Feb 2016
ANSC 4650 Comparative Immunology
Lecture 01: Introduction to Body Defense
- Maintain homeostasis
- Prevent pathogen entry into its body
oIf entry occurs, the host must
be able to restore
homeostasis by recognizing
the invading pathogen as
non-self and eliminate it
oDevelop long-term protection
against the pathogen
oIf unable to eliminate the
pathogen, disease will occur, leading to reduced productivity and possibly death
- Body also has non-pathogenic commensal microbial populations that reside on the epithelium of skin
and mucosal surfaces of the gastrointestinal, respiratory and urogenital tracts
oHost immune system learns to tolerate these microbes and are in a symbiotic relationship
Host provides nutrients and an environment that supports microbe survival
Microbes make nutrients available to the host and provide a level of protection against
invading pathogenic microbes
oIf immune tolerance to these microbes does not develop or is broken, can lead to disease
- Recognizing and responding to pathogens (non-self) and tumor cells (modified self) and tolerating non-
self commensal microbes is managed by the immune system
- Immune system is composed of two
arms = the innate and acquired
- Innate immune system
oAncient, highly conserved
- Acquired immune system
oArose much later during
evolution (525-652 MYA)
following activation of
recombination activation
genes (RAG1 and RAG2)
whose gene products are
enzymes that mediate the
first steps of B cell receptor and T cell receptor gene recombination
- Immunity: protection provided by the immune system to resist infection
- Humoral proteins and cells make up the immune systems, are effectors providing this protection
- Innate and acquired immune systems are not mutually exclusive as there are many cells and humoral
proteins that are involved in both immune responses
- Innate and acquired immune systems are tightly self-regulated and regulated by the neuroendocrine
system to ensure that they response efficiently and effectively to restore homeostasis
- Excessive and prolonged immune responses can lead to host tissue damage, leading to:
oChronic inflammatory disease
oDevelopment and proliferation of tumor cells
oSensitization to environmental antigens that lead to allergy
oSensitization to self-antigens that may lead to autoimmune disease
- Immune cells release immune signaling molecules called cytokines, and neuropeptides that bind to
their receptors to alert the CNS of danger could be considered the sixth sensory system
- Bidirectional communication among CNS and immune systems via the neuroendocrine-immune axis
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- Restricting microbial access and attachment to
epithelial cells is achieved by the presence of
physical and physiological barriers
oSloughing of non-viable epithelial cells
oMucous flow
oIncreased body temperature
oLow pH of the stomach
oAnaerobic GIT
oColonization of commensal microbes
along host epithelium
oPhysical processes (vomiting, diarrhea)
- If barriers are breached, immune cells and
humoral proteins making up the innate immune
system will provide immediate protection
- Innate immune response manifests as the host
inflammatory response and is triggered by
recognition of danger-associated molecular
patterns (DAMPs) by pattern-recognition
receptors (PRRs)
oThese DAMPs may include highly conserved pathogen-associated molecular patterns (PAMPs),
making up the microbial membrane, and host alarm signals (alarmins) that are released by
damaged host cells
- Innate immune response has limited specificity and does not provide long-term enhanced protection
- Inflammatory response is typically localized to site(s) of infection
oInfection can become systemic and potentially damaging if local defenses are breached, is then
called systemic inflammatory response syndrome (SIRS) which can lead to sepsis and death
- Acquired immune response is highly specific and provides long-term immunity
oTarget microbial proteins that bind as antigens by B-lymphocyte BCRs and T-lymphocyte TCRs
oCan manifest as a humoral antibody immune response (AbMIR) that targets extracellular
pathogens or as a cell-mediated immune response (CMIR) that targets intracellular pathogens
oTakes considerably longer for the host to mount an acquired immune response
Need sufficient inflammation to activate innate immune cells to a level where they will
process and present microbial antigens to antigen-specific lymphocytes in highly
specialized secondary lymphoid tissues
Antigen-specific lymphocytes activate, proliferate and differentiate into the effector cells
of the acquired immune system (e.g. T cells and antibody-secreting plasma cells)
Innate (always on) Acquired (induced by antigens)
History Ancient Recent
Onset Minutes-hours Days-weeks
Specificity Conserved molecular patterns (PAMPs) Specific antigens
Potency Can be overwhelmed Rarely overwhelmed
Memory Limited Long-term memory
Effectiveness Does not improve Improves to threshold with subsequent
Cell types Macrophages, DCs, granulocytes, NK
cells, γ δT cells, mast cells, epithelial cells
T and B cells, recruited macrophages, mast
cells, eosinophils
Effector humoral
Antimicrobial peptides, enzymes, natural
- Primary acquired immunity will occur over days-to-weeks to control and eliminate invading pathogen
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- Subsequent encounters with the invading pathogen will
result in a higher level of protection that is much more
efficient than the primary acquired response due to
specificity and memory
oEnhanced level of protection will reach a threshold
- Resolution phase: immune system is also involved in repair
and remodeling of damaged tissues
- During the AbMIR, innate immune cells act as antigen-presenting cells (APCs) that present antigens
from extracellular pathogens to antigen-specific T cells that
then activate antigen-specific B cells to proliferate and
differentiate into effector plasma cells to secrete antibodies
with effector functions
- During CMIR, APCs present antigens to antigen-specific T
cells which proliferate and differentiate into effector T cells
oThese effector T cells are recruited to the site of
infection during the acquired immune response
- Two whole genome duplication (WGD) events happened
between 794-652 MYA and 652-525 MYA, other WGD
events also occurred later that affected more specific
subsets of species
- These rounds of WGD are thought to result in new speciation events as unstable polyploidy genomes
reorganize time to again become diploid
- Gene duplication has contributed to:
oCopy number variation that effects mRNA expression
oDevelopment of pseudogenes that are utilized during BCR and TCR gene recombination
(important for their variation)
oDevelopment of non-coding RNA that are involved in gene regulation
oDevelopment of genes with slightly different or completely novel functions
Lecture 02: Physical Barriers at the Host-Microbial Interface
- Epithelial cells are at:
oRespiratory tract
oUrogenital tract
- Tightly joined together by adhesion molecules and tight junction
proteins, and are constantly replaced by underlying stem cells that
proliferate and differentiate
- Epithelial cells have a polarized morphology, with their apical side
exposed to commensal microbes and the environment, and their
sterile basolateral side protected from microbial exposure
oPRRs are concentrated on the basolateral side of the
epithelial cells and can tolerate commensal microbes on the
apical side, but also alert the underlying immune system of invaders and/or tissue damage
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