Mim - Lecture 8

Front 1

8.1

humoral immune response:

Back 1

- extracellular space protected by humoral immune response
- Abs produced by B cells cause destruction of external microorganisms and prevent spread of intracellular infections

Front 2

8.2

B cell activation:

Back 2

- humoral immune response
- Ag bound by surface immunoglobulin (BCR)
- internalize Ag -> degraded and processed
- peptide fragment presented on the B-cell attached to its MHC II
- armed helper T cells w/ TCR interacts w/ B cell -> signaling inside the Helper T cell
- cytokines are released and completes the activation of B cell

Front 3

8.3

Antibody secretion

Back 3

- humoral immune
- B cell activated to proliferate and differentiate into plasma (release Ab) and memory cell

Front 4

8.4

Adhesins:

Back 4

- cell surface bacterial molecules
- bind to cellular receptors on target cell surface
- endocytosis -> bacteria enters cell

Front 5

8.5

toxins:

Back 5

- adhesins for viruses
- 2 components
- 1 part bind a cellular receptor -> virus internalized
- other part released ijnto cytoplasm to poison the cell

Front 6

8.6

neutralization

Back 6

- 1 of the ways that antibodies prevent spread of infections
- antibodies prevent the pathogen and bacterial toxins from entering the cells by binding to adhesin molecules on their surface
- IgA (mucosal surface)
- IgG (within tissue)

Front 7

8.7

complement activation

Back 7

- one of the ways that Ab prevent the spread of infections
- antibody activates complement proteins which enhaces opsonization and/or lyses bacteria by activating enzymes that create pores in their membrane

Front 8

8.8

opsonization

Back 8

- a way that Ab prevent spread of infections
- alter the pathogen surface so it is targeted for ingestion by phagocytes
- antibodies coat pathogen by binding their cell surface adhesins
- Ab constant region recognized by Fc Receptors (FcR) on the surface of phagocytes (Macrophages)
- Ab + FcR -> phagocytosis

Front 9

8.9

virus-infected cells:

Back 9

- virus infected cells can communicate to the immune system by expressing viral molecules on their cell surface
- infected cell coated w/ antibody and recognized by FcRecptors (FcgammaRIII) on the surface of NK
- NK release cytoplasmic granules containing perforin and other enzymes to desotry the whole cell

Front 10

8.10

large parasites:

Back 10

- can't be ingested by phagocytes
- coated w/ IgE antibody
- constant region of the antibody is bound w/ high affinity to FceReceptor I (FceRI) on the surface of eosinophils -> release toxic from inside the eosinophils onto the surface of the parasite

Front 11

8.11

Ab-dependent cell-mediated cytotoxicity

ADCC

Back 11

- destruction of target cells by NK cell

Front 12

8.12

Thymus-dependent antigen:

Back 12

- activation of B-cell with the presence of T cell
- 2 signals are required
1) signal from BCR
2) Signal from armed Helper T cell

Front 13

8.13

Signal from armed Helper T cell

Back 13

- antigen is broken down and peptide is prosented on MHC II
- peptide is recognized by a helper T cell w/ TCR
- signal transmitted inside the helper T -> induce CD40 -> interacts w/ B cell's CD 40 adhesion molecule -> helper T cell to produce and secrete cytokines into surrounding area
- cytokines bind to a 2nd receptor on B -> B is activated

Front 14

8.14

armed helper T cell

Back 14

- have been primed earlier in the infection by immune cells such as macrophages or dendritic cells

Front 15

8.15

thymus-independent antigens:

Back 15

- thymus independent (TI) antigens, can activate B cells w/o signal from helper I -> signal is from the antigen itself

Front 16

8.16

TI-1 antigens

Back 16

- induce B cell activation in mature and immature B cell
- high doses of antigen: polyclonal activation: nonspecific antibody resonse
- low doses of antigen:L only interact with B cells that have specificity for the antigen: antigen specific resonse

Front 17

8.17

TI-2 antigena

Back 17

- no intrinsic B cell stimulatory activity
- can only activate mature B
- young children not good w/ this type of response

Front 18

8.18

mature B cell:

Back 18

can produce antibodies in the periphery

Front 19

8.19

immature B cell

Back 19

still developing in bone marrow

Front 20

8.20

linked recognition:

Back 20

- before B cell activation CD4 + T (helper) cell must be activated by interaction w/ MHC/peptide on DC or macrophage or B itself

Front 21

8.21

how B cells grow up:

Back 21

- develop in bone marrow to mature
- mature B travel through periphery -> lymph node -> primary follicle (white region of lymph node)
- some B activated here at B-T cell border
- B-cell form primary foci in medullary cords (region below T cell zone), but they eventually form the Germinal center

Front 22

8.22

Germinal Center:

Back 22

- if follicle contains a germinal center, it is no longer primary -> its now secondary follicle
- site where B proliferate and differentiates -> plasma and memory
- plasma -> bone marrow -> antibodies

Front 23

8.23

light zone (germinal center)

Back 23

- rapid B cell proliferation
- contain centrocytes

Front 24

8.24

dark zone (germinal center)

Back 24

- intense proliferation
- somatic hypermutation

Front 25

8.25

affinity maturation

Back 25

- selection of b cells that have high affinity for Ag binding and destruction of those that don't

Front 26

8.26

isotype switching

Back 26

- decline of IgM, rise in IgG
- IgM is the first that's produced