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Chapter 10 Dynamics of Adaptive Immunity. This chapter tries to integrate much of what we have already covered so we can better understand how the immune system protects from infection. How infectious agents cause disease The course of an adaptive immune response Immunological memory.

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slide1

Chapter 10

Dynamics of Adaptive Immunity

This chapter tries to integrate much of what we have already covered so we can better understand how the immune system protects from infection.

  • How infectious agents cause disease
  • The course of an adaptive immune response
  • Immunological memory
slide2

The course of a typical infection and adaptive immune responses can be divided into phases

If no innate immunity

slide3

The establishment of an infection depends on several factors:

  • Characteristics of the microorganism
  • Number of organisms
  • Mode of transmission (how and where they contact the host)
  • Stability of the organism (in and outside of the host)
slide4

Almost all infections begin at an epithelial surface*

Skin and tight junctions usually prevent penetration

*skin or mucosal surface of the respiratory, gastrointestinal, and urogenital tract which are always exposed to microorganisms.Interstitial tissues are normally free of any microorganisms (sterile)

slide5

Most pathogens have developed defenses to partially escape destruction by the innate protective mechanisms listed in boxes 1 & 2 below

Most pathogens cause disease in only one or a few related species because the pathogens can adhere to epithelial surfaces of only a few species or can escape innate immunity of only a few species.

slide6

The course of the adaptive response to infection

How do infections progress in immune deficient individuals?

Adaptive immune response becomes important when innate immunity cannot deal with the infection within a couple of day

slide7

The results of an immune response vary depending on the individual and the pathogen and other factors (e.g, level of care).

  • After a primary immune response, usually there are no pathogens remaining.
  • Sometimes the infection is contained but not elimintated (TB granuloma, herpes virus becomes latent, HIV mutates).
  • Sometimes the pathogen or the immune response, or both, leave significant tissue damage (e.g., scaring, blindness).
  • Often life-long immunity
slide9

NK1.1 T cell is a T cell sub-set which expresses a surface molecule usually associated with NK cells and do not express normal TCR repertoire

NK cell

TH1

TH2

What governs whether a TH0 cell differentiates into TH1 or TH2?

Pathogens influence cytokines that affect TH0 differentiation into TH1 or TH2

slide10

T cell subsets produce cytokines that regulate development of other subsets

For example, TH1 inhibits TH2 and TH2 inhibits TH1.

Thus most responses are dominated by either TH1 or TH2 and are not balanced responses

slide11

Cytokines influence the CD4 T cell subset development and this can be crucial for development of an appropriate immune response

Mice normally respond inappropriately to Leishmania and thus are killed by the parasite

slide12

Effector T cells change their adhesion molecules so they can migrate to the site of an infection. That is, adhesion molecules regulate trafficking

slide13

CD4+ T cells can license dendritic cells to activate CD8+ T cells (CTLs) (figure 8.28) but some CD8+ cells can be activated by dendritic cell in the absence of CD4+ T cells

CD8 T cells can be induced to secrete INF-g in an antigen non-specific way

slide14

Peripheral lymphoid organs are the site of antigen-specific B cell activation [antigen binding (signal 1) and T cell help (signal 2)]

The book is inconsistent on the location of the primary focus

slide15

Protective immunity is the resistance to a pathogen that results from infection or vaccination. It is due to an adaptive immune response which induced immunological memory of the pathogen. Usually, there are few or no symptoms associated with a infection when it is dealt with by protective immunity

Protective immunity consists of preformed immune components and immunological memory

slide16

No increase in specificity

Immunological Memory(maintenance of memory is probably antigen-independent but there is evidence for antigen sequestration or re-exposure to maintain memory)

Primary Vs. Secondary B Cell Responses

High quality

slide18

Affinity maturation

Affinity maturation is a form of somatic selection (somatic evolution) where B cells, using their surface antibodies (BCRs), compete for limiting amounts of antigen. The B cell must compete with each other and with free antibody produced by plasma cells or plasmablasts.

Only those B cells with the highest binding affinity will be able to bind to antigen and thus remain activated.

slide19

Some Characteristics of Memory B cells

Long-lived

Memory B cells have high affinity antibody and high levels of MHC so they are efficient at acquiring antigens (signal 1) and ready to get T help (signal 2)

Memory B cells have B7 on their surface so, maybe, they can activate or participate in activation of TH2 (memory) cells

Memory B cell have usually switch class from IgM so they usually have other Ig isotypes on their surface (mostly IgG)

slide20

Memory T cells remain long after the virus infection is under control* or the virus are gone

* The case shown here is the reactivation of a letent infection

slide21

Naïve and memory T cell have different requirements for survival

Naïve T cell require contact with MHC+self peptides for survival (like positive selection in the thymus)(too weak to activate the T cell)

Weak binding

Antigen encounter (signal 1) plus co-stimulation (signal 2) activates the T cell (proliferation and differentiation)

Strong binding

Memory cells can come directly from the activated naïve cells or from the effector cells

Some differentiate into effector cells

Strong binding

Memory cells need cytokines but not contact with MHC+peptide for survival. This is different from the naïve T cells (top panel)

Most effectors die in a few days

Memory T cells need MHC+self peptide to proliferate (weak interactions). These remain memory T cells and do not become effectors until they bind the MHC+the correct foreign peptide (strong binding).

Weak binding

slide22

Death

Plasma cell

Naïve B cell

Memory B cells

Effector T cell

Death

Naïve T cell

Memory T cell

slide23

We will skip subsets of memory cells (e.g. 10-17 and figure10.25

CD4 T cells are required for CTL (CD8) memory but not for primary CTL response

slide24

When antigens have both epitopes that were “seen” before and new epitopes, the memory responses to the epitopes seen before will dominate and there may be no response to the new epitopes

Original antigenic sin

Epitopes ABCD

Epitopes ACEF

Epitopes ADEG