1. erythema - due to increased blood flow
2. heat - due to increase in blood and more rapid metabolic processes
3. edema - increased permeability, fluid moves from blood to tissue spaces
4. pain - injury to nerve fibers or bacterial toxins

Increase Vasodilation

Increase Permeability

Released by mast cells in connective tissue - basophils in the blood

Intensify the effects of histamine

Released by injured tissue

Increase Permeability

Released by mast cells and basophils

Function in adherence of phagocytes to pathogens

• Released by monocytes, macrophages, lymphocytes
• Regulators of inflammatory response
• Attract leukocytes, initiate fever

• Increase Vasodilation
• Increase Permeability
• Stimulates histamine release
• Attract neutrophils
• Promotes phagocytosis

Basophils, neutrophils, eosinophils, mast cells

Destroy intracellular pathogens (phagocytosis), release chemicals

Macrophages, monocytes, dendritic cells

Present antigens to lymphocytes

Short lived
Ingest, kill, and digest microbial pathogens
First to inflammatory sites
Granules contain antimicrobial agents, such as:

1. lysozymes
2. lactoferrin

Mast cells are tissue counterpart

Produce cytokines in defense against parasites

Responsible for allergic reaction

Secrete primary mediators (histamines) and secondary mediators (leukotrienes)

Macrophages are tissue counterpart

Phagocytosis and intracellular killing

Antigen presentation to T-cells

Recruit other immune cells through cytokine and production

Specialized Macrophages:

1. Kupfer cells (liver)
2. Glial cells (brain)
3. Langerhans cells (skin)
4. Osteoclasts
5. Alveolar macrophages

these are differentiated macrophages that act as APCs to active T-helper cells, Cytotoxic T cells, B-cells

Found in most organs

Differentiate into plasma cells to secrete immunoglobulin glycoproteins that bind antigens with high degree of specificity

immature thymocytes differentiate in the thymus

cell mediated immunity

help B-cells produces immunoglobulins

CD4 expressing T helper cells

CD8 expressing Cytotoxic T cells

• T-Helper Cells
• Regulators of delayed-type hypersensitivity responses
• Assist in the stimulation of B cells

Cytotoxic T cells

Cytotoxic against tumor cells and host cells with intracellular pathogens

Large, granular lymphocytes

Kill tumor cells and pathogen-infected cells

Enhanced by IFN and IL

Lack the major B and T-cell markers

Kill by direct and antibody-dependent cytotoxicity

• Has vascular sinuses with macrophages
• Macrophages break down old RBCs and recycles hemoglobin - retrieval of iron
• Macrophages also break down platelets

• T and B cell area
• Germinal centers w/ macrophages and dendritic cells --> present antigens to lymphocytes
• B-cells become plasma cells so they can make immunoglobulins
• Macrophages break down antigens

Filters antigen and debri from lymph

Macrophages and dendritic cells (primarily in medulla area) cleanse lymph

T cell and B cell maturation occurs here

Tonsils

Peyer's Patches (located in ileum)

Appendix

• These are cellular aggregates (non-encapsulated) in the lining of the respiratory and digestive tracts
• They are strategically located to recognize antigens and respond with an appropriate immune response
• Contain resident intraepithelial lymphocytes

• This is a form of SCID (Severe Combined Immunodeficiency)
• An autosomal recessive disorder
• Absence of germinal centers in lymph nodes --> replaced with a diffuse infiltrate of large cells with abundant cytoplasm
• There is abnormal intra-thymic T-cell development plus inefficient and/or abnormal generation of TCR's as well as a deficiency of B-cells and receptors (antibodies)

Chronic diarrhea

leukocytosis

1. Express the CD4 co-receptor
2. Recognize antigens complexed with MHC II on B cells, macrophages, or other APCs
3. Activate memory T helper cells and cytokine-secreting cells
4. Stimulated B-cells

1. Express the CD8 co-receptor
2. Dependent upon MHC I on APCs
3. Are cytotoxic against tumor cells
4. Are cytotoxic against host cells with intracellular pathogens --> causes them to undergo apoptosis

1. T-cell receptors
2. B-cell receptors
3. MHC

False

ALL TCR's expressed by a SINGLE T-CELL ARE SPECIFIC for the SAME ANTIGEN

MHC I are associated with this type of antigen processing

MHC I are found in all nucleated cells (excluding immunological cells)

MHC I participates in anitgen presentation to CD8 Cytotoxic T cells

Endogenous because the virus has already infected the cell and has started to make viral proteins that are in the cytoplasm (endogenous pathogens)

The viral protein is degraded by proteosomes and the degradation products of the viral protein are combined with MHC I --> sent to cell surface for presentation

This marks the cell for destruction by Cytotoxic T cells

• MHC II are associated with this type of antigen processing
• MHC II molecules are found on APC's (macrophages, dendritic cells) and B-cells
• MHC II participates in antigen presentation to CD4 T-Helper cells
• Exogenous because the pathogen is outside the cells and is taken up by endosomes that break it down
• The degradation products will be combined with MHC II and sent to the surface of the cell for presentation

1. Drop in BP
2. Shock
3. Fever
4. Blood clotting

endotoxin stimulation of macrophages after G- bacterial infection --> septic shock

Immune suppression

Caused by Trypanosoma cruzi --> Chagas

With IgM, it the major Ig expressed by mature B-cells

Functions in activation of B-cells by antigens

• Protects fetus
• Neutralizes bacterial toxins and viruses
• Complement activator
• Plays a huge role in persistent viral, bacterial, and fungal infections

Binds to allergens

Mediates hypersensitivity reactions (such as asthma, hives, hay fever) by inducing degranulation of basophils and mast cells

Protects against parasitic infections

• Analagous to neutrophils in that they are the first to respond to an infection
• Has 10 antigen binding sites
• Activates complement pathway

1. Antigen recognition
2. Lymphocyte activation
3. Effector Phase
4. Decline (homeostatis)
5. Memory

• Cancer of the cells in the bone marrow --> results in an increase in plasma cells
• There will be a decrease in polymorphonuclear cells

• They have a marked increase in plasma cells, which results in an increase in IgG and they are producing only that particular Ig
  Their body is not producing any other Ig (such as IgA, IgD, IgM, etc.)
• This leaves the patient susceptible to other pathogens that other Ig take care of (parasites, no added protection of IgA in tears, etc.)

1. Alternate (innate) pathway
2. Classical (humoral) pathway

Adaptive (humoral)

• It is activated by antigen/antibody complexes containing IgM or IgG
• It is the major effector of the humoral immunity

1. Membrane Attack Complex acts as a molecular drill to puncture cell membranes
2. Complement cleavage products promote: opsonization (enhancement of phagocytosis) inflammatory responses, degranulation, etc.

• Deletion of a portion of chromosome 22
• Babies are born without a thymus

• Basically, patient will not have maturation of T-cells, because this is where T cells mature
• Since the baby does not have a thymus, its body will rely on bone marrow
• However, T-cells will not have their coreceptors (CD4 or CD8) and therefore no T-helper cells or Cytotoxic T cells
• There will be an accumulation of B cells that won't be stimulated