Final Exam- Animal Health and Disease Control

Texas State AG 3314 Spring 2025

Imunology

The study of white blood cells

Disease

Disfunction of a normal body condition.

Hematopoesis

production of white blood cells

Leukocytes

Mast cells, eosinophils, basophils, neutrophils, macrophages, dendritic, natural killer cells.

Lymphocytes

B cells and T cells

Granulocytes WBCs

mast cells, eopsinophils, basophils, neutrophils

Phagocyte WBCs

neutrophils, macrophages, dendritics

Antigen Presenting WBCs

Macrophages and dendritic

Chemokines

tells cells WHERE to GO

Cytokines

tells cells WHAT to DO

Mast Cells

Granulocyte, causes vasodilation (histamine), contains one nucleus

Eosinophil

Granulocyte, bliobed nucleus, heavily granulated, low quantities, high in parasitic response.

Basophil

Granulocyte, bilobed nucleus, heavily granulated, found in low quantities, respiratory and allergy response

Neutrophil

Granulocyte and phagocyte, 3 nuclei, most abundant WBC (50-75%), first WBC to the site of infection, major role in inflammatory response. apoptocizes and macrophage comes and engulfs.

Macrophage

Phagocyte and APC, largest WBC, great at phagocytosis, secretes cytokines and chemokines

Dendritic

Phagocyte and APC, great at activating adaptive immunity

Primary lymphatic organs

Synthesis and maturation. Bone marrow and Thymus gland.

Bone marrow is site of hematopoiesis

The medulla of the thymus gland is the site of T Cell, macrophage and dendritic cell development

Secondary lymphatic organs

Storage of mature WBCs. Spleen and lymphnode

The red pulp of the spleen is the site of storage for macrophages and dendritic. T cells stored in the white pulp.

Paracortical area of the lymphnode houses T cells, primary lymphoid follicle houses B cells

Bone marrow is the site of

Hematopoeisis

Site in thymus that develops macrophages, dendritic and T cells

Medulla

Site of spleen that stores macrophages and dendritic cells

Red pulp

Site of spleen that stores T cells

White pulp

Site of T cell storage in lymphnode

Paracortical area

Site of B cell storage in lymphnode

Primary lymphoid follicle

First step of Phagocytosis

PRRs on phagocytes recognize pathogens PAMP

Second step of Phagocytosis

Ingestion of pathogen and formation of phagosome

Third step of Phagocytosis

Lysosome and phagosome fuse together to form Phagolysosome

Step four in Phagocytosis

Microbial breakdown of pathogen using lysozymes

Step five in Phagocytosis

Apoptosis via neutrophils, exocytosis, or antigen presentation on the MCH II complex.

On bacteria or viruses, how do WBC recognize the pathogen?

It’s PAMP

Pathogen Associated Molecular Pattern.

How do leukocytes recognize a pathogen?

It’s PRR

Pathogen Recognition Receptors.

What is the inflammatory response?

Occurs when there is tissue damage or via a pathogen. Can result in itching, swelling, fever/heat, redness and pain. It can be acute or chronic

First step in the inflammatory response.

Cell damage causes cell to release signaling proteins. Pathogen releases endotoxins.Damaged cells release a protective proteins to warn neighboring cells

Second step in the inflammatory response.

Mast cell becomes activated by recognizing endotoxins or the protective proteins.

Third step in the inflammatory response.

Mast cells degranulate and release histamine that targets the capillary wall. This causes vasodilation.

Fourth step in the inflammatory response

Preformed granules in capillary cells are mobilized to cell surface to for

P-selectins

Fifth step in the inflammatory response

Chemokines that are released from damaged cells enter circulation to recruit neutrophils and monocytes (macrophages precursor. in circulation not in tissue yet)

Sixth step in the inflammatory response

Sugar molecules on neutrophils and monocytes allow for marginalization (movement) on P-selectins

Seventh step in the inflammatory response

Neutrophils and monocytes squeeze through capillary walls at vasodilation. This is called diapedesis. Neutrophils and macrophages are at site of the infection.

Eighth step of the inflammatory response

Complement system activated and is killing via MAC. Neutrophils phagocytosing pathogens and die via apoptosis. Dendritic cells are phagocytosing and presenting antigen on MHCII

Ninth and final step of the inflammatory response

Cytokines go to nearest lymphnode to activate T and B cells to trigger the adaptive immunity.

The Complement System

Three pathways: classical, alternative and lectin.

Classical pathway step 1:

Antibody on pathogen is recognized by the (non specific) FC portion.

Classical pathway step 2:

C₁ recognizes FC portion of the antibody

Classical pathway step 3:

C₄ binds to C₁

Classical pathway step 4:

C₂ binds to C₄

Classical pathway step 5:

C₃ binds to C₂

Classical pathway step 6:

C₅ binds to C₃

Classical pathway step 7:

C₃ and C₅ are cleaved by convertase into C₃b+C₃a, and C₅b+C₅a

Classical pathway step 8:

C₃b and C₅b stay attached to the system, C₃a and C₅a become chemokines

Classical pathway step 9:

C₆-C₉ bind to C₅b

Classical pathway step 10:

C₅b→C₉ break off and become MAC attack complex

MAC: membrane attack complex

Classical pathway step 11:

MAC attaches to pathogen and allows for Na²⁺ and H₂O to enter pathogen. This causes lysis and kills the pathogen.

Alternative pathway step 1:

C₃ and C₅ attach directly onto pathogen

Alternative pathway step 2:

C₃ and C₅ cleaves into C₃b+C₃a, and C₅b+C₅a. b’s stay and a’s become chemokines

Alternative pathway step 3:

C₆-C₉ bind to C₅b

Alternative pathway step 4:

C₅b -C₉ break off and form MAC.

Alternative pathway step 5:

MAC allows for Na²⁺ and H₂O to come in and allow lysis

Alternative pathway step 6:

Macrophage phagocytosis

Lectin pathway step 1:

Lectin binds to manose molecule on a pathogen

Lectin pathway step 2:

C₄ binds to Lectin, C₂→ C₄, C₃→C₂, C₃→C₅

Lectin pathway step 3:

C₃ and C₅ cleave C₆-C₉ bind, break off and form MAC

Lectin pathway step 4:

lysis→ macrophage phagocytizes

Antibodies

produced by plasma B cells. Consist of the heavy chain and light chain. With constant regions that determine isotope. Variable regions are the specific portion of antibody

IgG

monomer structure, most abundant, passive immunity, passes through the placenta, highest in 2nd response, good and neutralization and precipitation, opsonin.

IgA

Dimer structure, found abundantly in mucus membranes (GALT, MALT, BALT), passive immunity, passed through colostrum, good at neutralization and agglutination.

IgM

2 forms, membrane bound B cells and pentomer, highest in primary response, because it has 10 epitopes (if pentomer) and yet to gain memory, primarily agglutination.

IgE

Monomer structure, found in respiratory and GI tract, part of allergies, FCεR1 on mast cells and IgE’s recognize, essential to the parasitic response.

IgD

Monomer, membrane bound only→ B cell receptor, determines stage in B cell development.

Neutralization

Antibodies bind to pathogen, neutralized pathogen

Agglutination

Collects whole pathogens together

Precipitation

Clumping of free floating antigens

Cell mediated toxicity

IgG’s!! when cells are sick (IgG’s work with NKC) or have parasites (IgE’s work with eosinophils) used when phagocytosis isn’t an option.

B cell development

beings in the bone marrow, finishes in lymphnode to be activated. 2 stages antigen independent and antigen dependent. Remember the six stages: Happy PROfessors PREpare Interesting Notes Meticulously

Step 1: Hematopoietic Stem Cell

Happy

Stromal cell expresses VCAM1. Hematopoietic stem cell binds with VCAM1 using its VLA4 receptor.

Step 2: Progenitor B Cell

PROfessors

recombination of the heavy chain. stromal cell expresses SCF. Pro B cell recognizes SCF with its KIT receptor. This causes the expression of IL7 receptor on Pro B cell and release of IL7 of stromal cell. IL7 causes the recombination of Heavy chain

Step 3: Pre B Cell

PREpare

After breaking off from stromal cell, the heavy chain is expressed on the cell membrane with surrogate light chain

Step 4: Immature B Cell

Interesting

Testing for autoreactivity (attacking self cells) in 2 stages.

Central tolerance autoreactivity testing

In bone marrow, testing the IgM with stromal cells, HSC and blood plasma proteins, if autorective, the surrogate L.C. recombines or apoptosis via clonal deletion or anergy

Peripheral tolerance autoreactivity testing

In spleen and lymphnode because not all self cells are in the bone marrow, tests with tissues and secreted/surface proteins. If autoreactive, apoptosis.

Step 5: Naive B Cell

Notes

Antigen dependent and now in the lymphnode. IgM and IgD are expressed

Step 6: Mature B Cell

Meticulously
Differentiation stage, into memory of effector plasma B cells

T Cell Development

7 steps: The PROud Prince Never Doubts Nobility & Majesty

Step 1: Thymic Cells

The

Thymic cells secrete cytokines to recruit hematopoietic stem cells to thymus

Step 2: Progenitor T cell

PROud

Recombination step, chemokines act on the Pro B cell, targets RAG₁ and RAG₂. this creates the T cell receptor, results in cluster differentiation proteins CD8 and CD4

Step 3: Positive selection

Prince

Thymic cell presents both an MHCI and MHCII. CD8 binds to MHCI and CD4 binds to MHCII. If not recognized, to right CD/MHC results in apoptosis

Step 4: Negative selection

Never

recognition of self antigens. testing TcR against self antigens on MHC’s. If autoreactive, apoptosis

Step 5: T Cell Differentiation

Doubts

where T cells get their jobs! completely random, become helper T cell (Th) or cytotoxic T cell (Tc). If MHCI binds to CD8→Tc, if MHCII binds to CD4→Th

Step 6: Naive T cell

Nobility

Travels to secondary lymphoid organs waiting for activation

Step 7: Mature T cell

Majesty

Activated! proliferates into effector Tc or Th cells/ memory Tc or Th cells

Cytotoxic T cells

Causes apoptosis in cancerous/ infected cells by releasing granulozymes and perforins

Helper T cells

Help with activation of B cells. produce cytokines.

Th Activation

1. Recognition of antigen on the APC (dendritic). Th CD4 recognizes MHCII on APC and antigen

2. Costimulatory protein CD28 from Th binds with costimulatory receptor CD80 on APC.

3. Th releases IL2 and binds to their own Th IL2 receptor. Th can now proliferate into effector/ plamsa or memory Th cells.

Ways B cell can be stimulated

1. Th dependent:

   a. bind to a free floating antigen

   b. APC from dendritic cell

   c. B cell recognizing whole pathogen

2. Th independent:

   requires APC from Th

Step 1 in the humoral response

Th activation! either from recognizing antigen on APC and CD4 with MHCII on dendritic, Th CD28 binds to APC’s CD80 or, IL2 from Th released and Th’s IL2 receptor.

Step 2 in the humoral response

Naive B cell stimulation.

If nonprotein antigen: free floating antigen, whole pathogen or APC from dendritic

If protein antigen: Th stimulation

Step 3 in the humoral response

Th activates Naive B cell. ThR and CD4 recognize MHCII on naive B cell receptor. causes expression of the CD40 ligand on the Th and CD40 receptor on Naive B cell. Th releases IL5. This happens no matter what.

Isotope switching

process of switching IgM into variety of immunoglobulins. must encounter an antigen, irreversible process, changing the constant region on the antibody. on chromosome 14. activated induced deaminase knows which regions to splice (switch regions) variable portion of heavy chain called variable diversity joining (VDJ)

IgM → Cμ

IgD → Cδ

IgG →Cγ3, Cγ1, Cγ2b, Cγ2a

IgE → Cε

IgA →Cα

Hypermutation

Affinity maturation, natural selection for B cells, changes strength, if still not “strong enough”, B cell is killed

Cell mediated immune response

Cells helping sick cells. Key players Cytotoxic T cells (specific) NKC (nonspecific). They recognize differently but kill the same.