L18-Immunology (28) Flashcards

http://www.youtube.com/watch?v=h5oOUMP4_UM Immune response-Bacterial Infections

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1
Q

Describe the development of different types of leukocytes.

A

Bone marrow stem cell can become myeloid (innate) or lymphoid (active) precursor. Myeloid can become monocytes (APCS-dendritic or macrophage) or granulocytes (neutrophil or mast). Lymphoid can become T cell (thymus) or B cell (bone marrow), which can later become a plasma cell.

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2
Q

Define: MHC.

A

Assists in antigen presentation. Every host cell has major histocompatibility complex proteins (MHC) and antigen presenting cells have MHC II.

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3
Q

Describe innate immunity.

A
  • nonspecific
  • does not require previous exposure to pathogen
  • mediated by phagocytes, PRR bind to PAMPs, use cytokines to recruit more phagocytes
  • recruit other immune cells for adaptive immunity
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4
Q

Define: PRR, PAM.

A

pattern recognition receptors and pathogen-associated molecular patterns.
Phagocytes have pattern recognition receptors (PRRs) on cell membrane. When PRR interact with a pathogen-associated molecular pattern (PAMP), phagocytosis is activated.

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5
Q

What is the adaptive immune response?

A
  • acquired ability to recognize and destroy an individual pathogen (antigen-specific)
  • pathogen specific receptors are produced AFTER exposure to pathogen or its product
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6
Q

Explain the process of antigen presentation to T cells.

A

1) Phagocytosis of the pathogen
2) presents antigen (part of digested pathogen) on MHC I and II
3) T-cell receptors TCR interact with MHC and antigen
4) Leads to T-cytotoxic produce perforin/granzymes to lyse nearby target cell or CD4 T-helper produce cytokines to activate other cells, inflammation.

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7
Q

Describe antibody structure and function.

A
  • soluble protein made by B and plasma cells
  • binds to a specific antigen and marks for destruction
  • can also block interactions between pathogens or their products and host cells (neutralization)
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8
Q

At the molecular level, what cause the wide diversity of antibodies?

A
  • V(D)J-variable, diverse, joining recombination
  • heavy and light chains have constant and variable chains encoded by genes on 3 loci
  • VDJ portions randomly recombined for heavy chains
  • VJ portions randomly recombined for light chains
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9
Q

How are pathogens targeted for destruction by antibodies?

A

1) Antibodies binds to a specific antigen.
2) Complement (group of proteins) attach to pathogen surfaces and create pores for lysis or block pathogen toxins/interactions
3) neutrophil/macrophage Fc receptors bind antibodies or complement to enhance phagocytosis (opsonization)

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10
Q

List the different types of immunoglobulins and their function.

A

IgE-immediate hypersensitivity allergies, parasite immunity (bound to mast cells)
IgA-mucosal immunity (serum/mucus secretions)
IgG-(serum) secondary
IgM-(serum) primary

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11
Q

What is immunological memory and how is it created?

A

defn-creation of database of antibodies for mounting larger secondary responses after antigen reexposure

1) B cells (preformed antibodies), bind antigens using Ig.s,
2) presents antigens to TH2 cells.
3) TH2 cells produce cytokines to stimulate growth of B cells into plasma cells
4) plasma cells produce antibodies.

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12
Q

What is the purpose of inflammation in the immune response?

A

rapid localization and destruction of the pathogen by macrophages and recruited neutrophils

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13
Q

Define: tolerance and autoimmunity.

A
  • tolerance: acquired inability to produce an immune response to a specific antigen
  • autoimmunity-T cells and B cells react with self antigens (normally eliminated during process of lymphocyte maturation), lead to disease
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14
Q

Describe the difference between active and passive immunity. Give examples of each.

A

active-exposure to antigen through infection, protective immunity ex. common cold, natural infection
passive-non-immune, person’s acquisition of preformed immune cells or antibodies via natural transfer ex. IgG antibodies through placenta, IgA from breast milk

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15
Q

How do super antigens work?

A

activate more than normal 20-25% T cells via non-specific binding of antigen, Ex. Staph aureus food poisoning and Strep pyogenes scarlet fever

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16
Q

Give examples of different types of immune diseases.

A
  • type I juvenile diabetes-TH1 mediated autoimmune attacks B cells
  • Hashimoto’s disease-autoantibodies against thryoglobulin
  • severe combined immunodeficiency (prevents formation of expression of antibodies/TCR)
17
Q

Describe mechanism of inflammation.

A

1) PRR engages PAMS on pathogen
2) activation of macrophages to release cyto/chemokines (ex. CXCL8, neutrophils chemokine gradient)
3) cyto/chemokines such as IL-1, IL-6, tumor necrosis factor a contribute to inflammation

18
Q

What causes systemic inflammation and septic shock?

A

1( inflammatory response fails to localize the pathogens

2) inflammatory cells and mediators contribute to inflammation of entire circulatory/lymphatic systems
3) can lead to septic shock, life threatening
- ex. Salmonella or E. coli ruptured or leaking bowel