Immunology Flashcards by Madison Warner

Innate immune defenses

Epithelial barrier: Skin, respiratory epithelium, enterocytes
Secretions: Mucus, sweat, sebum, cerumen, acid, enzymes, defensins, polyreactive antibodies, surfactant
Endogenous microflora
Resident phagocytes
Pattern recognition receptors (PRR)

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cell mediated immune response

Mediated by Th1 cells
Most important for intracellular pathogens

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humoral immune response

Mediated by Th2 cells
Most important for extracellular pathogens

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How viruses infect cells

Bind to cell receptor (adsorption)
Virions enter cell
Nucleic acid released into cytoplasm
Replication
Protein production
Assembly
Release
Spread

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What triggers the innate immune response to viral infection?

Recognition of viral patterns by PRRs
RIG-I, MDA5 (cytoplasmic)
**TLR3, 7, 8, 9 **(endosomal)

Cell damage

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interferons

Glycoproteins, Regulate protein expression
Three types
* Type I
IFNa – dendritic cells
IFNb – any virally infected cell
* Type II
IFNg – activated Th1 cells
* Type III
Various - mucosal epithelial cells

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type 1 interferons

IFNa – dendritic cells
IFNb – any virally infected cell
Produced upon recognition of TLR7 or TLR9 ligands

Activate JAK/STAT pathways
* Increased production of antiviral and immunoregulatory proteins
* Directly inhibit viral uptake, replication
* Induce apoptosis

Produced within hours (before antibodies), part of innate immune system

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humoral immunity in viral infections

Antiviral antibodies against viral proteins
Antibody binding prevents viral infection by
* Blocking viral invasion
* Stimulating phagocytosis
* Triggering complement-mediated virolysis
* Promoting viral clumping
* NOT by direct virus destruction

ADCC targets infected cells for destruction
* NK cells and cytotoxic T cells

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cell mediated immunity in viral infections

Cytotoxic T cells recognize infected cells prior to rupture
* Induce apoptosis
* Recognize peptide-MHC-I complexes and kill cells
* Sensitized by type I interferons

Macrophages are activated by Th1 cells
* Phagocytosis

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immune evasion by viruses

RNA viruses rely on antigenic variation
DNA viruses – immunoregulatory genes
* Proteins that block IFN signaling
* Proteins that interfere with MHC-I associated antigen presentation
* Evasion of NK cells
* Alterations in humoral immunity: Non-neutralizing or slowly neutralizing antibodies
* Antigenic variation

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antigenic variation

Point mutations + poor editing
Sporadic recombination of strains
ex: Influenza A
* Express envelope proteins: Hemagglutinins (HA), Neuraminidases (N)
* Gradual variation in amino acid sequence leads to new antigens
* Co-infection leads to new strains
* No longer recognized by adaptive immune system

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innate response to bacteria

Bacteria are recognized through PRRs (TLR1, 2, 4, 5, 6, 9)

Cytokine release,** complement** activation, inflammation, phagocytosis

Sequestration of nutrients (iron, tryptophan)

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PRRs for bacteria

TLR1, 2, 4, 5, 6, 9 (9 is both)

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adaptive immune response to bacterial infections

Extracellular bacteria = humoral immunity
* Neutralization of toxin
* Opsonization by antibodies
* Killing by classical complement pathway
* Phagocytosis by activated macrophages

Intracellular bacteria = cell mediated immunity
* Macrophage activation and killing
* Destruction by cytotoxic T cells

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adaptive immune response to bacterial infections

Extracellular bacteria = humoral immunity
* Neutralization of toxin
* Opsonization by antibodies
* Killing by classical complement pathway
* Phagocytosis by activated macrophages

Intracellular bacteria = cell mediated immunity
* Macrophage activation and killing
* Destruction by cytotoxic T cells

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neutralization

Important for toxogenic bacteria

Antibodies generated against toxins:
* Bind
* Prevent interaction with receptor
* Can be IgG or IgA (mucosal surfaces)

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opsonization and phagocytosis

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Opsonization increases efficiency of phagocytosis (natural ketchup)
Antibodies against surface antigens
Bacteria coated in antibodies and complement fragments are primed for phagocytosis
IgM is the most efficient antibody in opsonization

destruction by activated macrophages

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Some bacteria can replicate inside macrophages
Th1 cells activate macrophages by secreting IFNg
Acidification of phagosomes
Intracellular bacterial destruction
NK and cytotoxic T cells can also kill cells infected with intracellular bacteria

destruction by activated macrophages

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bacterial evasion of innate defenses

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Interfere with TLR signaling
* Modify PAMPs (molecular patterns)
* Interfere with intracellular signaling

**Resistance to antibacterial peptides **
**Block phagocytosis **

Intracellular bacteria
* Interfere with phagosomal maturation
* Escape phagosome

bacterial evasion of adaptive defenses

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Antigenic variation
Secrete proteases to destroy antibodies or cytokines
Survival within macrophages
Interference with macrophage polarization

TLRs that recognize viruses

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3, 7, 8, 9 (9 is both)

parasites

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Organism that lives in/on host and gets nutrients from the host or at the expense of the host
Three categories of eukaryotic parasites
* Protozoa – single-celled, intra- or extracellular
* Helminths – multicellular, extracellular
* Arthropods – multicellular, extracellular

Immune response to protozoa

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Innate mechanisms similar to bacteria and viruses
Mutual adaptation and species-specific infection is important
* Toxoplasma in cats vs. other mammals

Stimulate both cell mediated and humoral response
* Humoral – antibodies opsonize parasites in blood and tissue
* Cell mediated is important for intracellular protozoa

extracellular protoza immune response

Similar response to bacteria * **Complement** activation * Activation of **macrophages for phagocytosis** **Th22** responses are important * **Macrophages** produce **IL-22** Recruitment of **neutrophils** * **Oxidative damage** to pathogen

intracellular protozoa immune response

Intracellular location protects organisms from immune detection Some actively penetrate cells * Toxoplasma sp., Cryptosporidium sp. **Th1 responses** are important * Recruitment of **cytotoxic T cells**

immune evasion by protozoa

**Parasite-induced immunosuppression** * Secondary infections and sepsis Reduced antigenicity of **encysted** protozoan **Antigenic variation** Infections more common in immunosuppressed hosts

adverse consequences of immune reponse to protozoa

Immune response to protozoa may result in **hypersensitivity** Type I: Trichomoniasis infection causes **local irritation of genital tract** Type II: Parasite **antigens bind to host erythrocytes** Type III: **Immune complex formation** in visceral leishmaniasis

immune reponse to helminths

Larvae and adults trigger **Th2 adaptive response** * Attacked by **eosinophils** and basophils Adult worms are expelled from mucosal surface by **IgE** binding * Cell mediated immunity less important * Innate immune cells and **Th2** cells secrete **IL-4, IL-5 and IL-13** * Increased production and recruitment of **eosinophils** * Eosinophils have **Fc receptors and bind to opsonized worms** Thick cuticles or tegument * Complement and perforin (cytotoxic T cells) will not penetrate * If outer covering is damaged, they can grow a new one **Eosinophils and macrophages release Th2 cytokines – cuticle damage** * important in destroying migrating larvae **Similar clinical signs to type I hypersensitivity**: (Eosinophilia, Edema, Asthma, Urticaria)

helminth immune evasion

**Migrating larvae** are very good at immune evasion Innate immunity * Neutrophil inhibitors * Surface antioxidants * Interfere with complement Adaptive immunity * Reduced antigenicity over time * **Antigenic variation** * Interference with antigen processing

immunosuppression by parasites

Common feature of parasitized animals **Parasites produce immunosuppressive molecules** * ex: Fasciola hepatica proteases can destroy antibodies Redirection of T cell response * Produce **IL-10** which is immunosuppressive

immune response to arthropods

Fleas, ticks, mosquitos, mites, lice Inject saliva * Digestive enzymes * Immunomodulatory substances Three types of response * **Th1** response * **Th2** response * **Cutaneous hypersensitivity**

immune response to fungi

Innate immune response * **PRRs** recognize fungal PAMPs * **Neutrophil** recruitment – moderately effective * Small spores may be ingested by **macrophages** Adaptive response * **Th1 most important** * Activated **macrophages** * **Neutrophils**

Enzyme Linked Immunosorbant Assay (ELISA)

1. add serum that has antigen, binds to captured antibodies 2. add labeled/detection antibodies 3. add substrate 4. signal detection

monoclonal antibodies

react to one antigen

polyclonal antibodies

Reacts to many antigens expressed by a certain pathogen

snap tests

1. precoated capture antibodies on matrix 2. add serum/conjugate, antigen binds to capture antibodies 3. wash antibodies that are not bound 4. substrate moves across matrix making color

immunohisochemistry

1. primary antibody targets protein 2. direct: enzyme on primary antibody 3. indirect: secondary antibody binds to primary antibody 4. gives off a color

agar gel diffusion assay

Test for **antigen-specific antibody** in test serum Wells in a gelatinous matrix Known antigen in middle well Serum from control and possibly infected animals in peripheral wells Look for lines of precipitation

COVID 19 rapid antigen test

Antigen binds to detection antibody The complex migrates and is captured by antibody coated in the test band area Control antibody only recognizes the detection antibody (not antigen)

Immunology Flashcards

(40 cards)