Secondary Immune Response

- Purvi Gosrani

IntroductionA secondary immune response is a response to an illness that has occurred for the second time

It activates previously generated memory cells

Secondary immune response is different from the primary response, both qualitatively and quantitatively

The log phase in secondary response is very short or negligible

Lag face is absent in secondary response

Raise of antibody concentration is about 100 to 1,000 fold higher than the primary response resulting a short log phase

1° Immune Response

1. Following the first exposure to a foreign antigen, a lag phase occurs in which no antibody is produced, but activated B cells are differentiating into plasma cells. The lag phase can be as short as 2-3 days, but often is longer, sometimes as long as weeks or months.

2. The amount of antibody produced is usually relatively low.

3. Over time, antibody level declines to the point where it may be undetectable.

4. The first antibody produced is manily IgM (although small amounts of IgG are usually also produced).

2° Immune Response

1. If a second dose of the same antigen is given days or even years later, an accelerated 2° or anamnestic immune response (IR) occurs. This lag phase is usually very short (e.g. 3 or 4 days) due to the presence of memory cells.

2. The amount of antibody produced rises to a high level.

3. Antibody level tends to remain high for longer.

4. The main type of antibody produced is IgG (although small amounts of IgM are sometimes produced).

Immunological Memory Is Sustained By Clones Of Long Lived Memory T Cells

And B CellsAfter the level of pathogen-specific antibody made during a primary immune response has declined, immune defences relaxed and the potential for that pathogen to re-establish an infection increases

During a primary immune response, the clonal expansion of pathogen-specific T cells and B cells gives rise both to short lived effector cells that work to stop the infection and to long-lived memory T cells and memory B cells

In the secondary immune response, these memory cells are activated by antigen to proliferate and differentiate into effector cells

Several factors contribute to this difference: memory cells are more sensitive to infection, more easily activated, and more abundant than naive lymphocytes specific for the same pathogen

Memory B cells have also undergone isotype switching and affinity maturation and so will produce more effective antibodies than IgM made at the beginning of the primary infection with the pathogen

Vaccination Against A Pathogen Can Generate Immunological Memory That

Persists For LifeThe goal of vaccination is to immunize people with a benign form of a pathogen and induce immunological memory

Any infection with the real pathogen will meet a secondary immune response that terminates the infection before it causes disease

Smallpox virus was once an effective killer of humankind: from 1850 to 1979

About 1 billion people died from smallpox

Worldwide vaccination programs progressively reduced the spread of the virus to the point at which in 1972 mass vaccination was discontinued in the United States and in 1979 the smallpox virus was eradicated worldwide

Pathogen–Specific Memory B Cells Are More Abundant And Make Better Antibodies Than Do

Naive B CellsIn primary infection, proliferation and differentiation of antigen-specific naive B cells produces large numbers of antibody – secreting plasma cells

A smaller number of memory B cells to deal with future infections

The first antibodies to be made in the primary response are low – affinity IgM

As the response proceeds, somatic hypermutation, affinity maturation, and isotype switching give rise to high-affinity IgG, IgA, and IgE

Memory B cells are derived from the clones of B cells making the highest-affinity antibodies

On a second infection, 10-100 times more pathogen-specific B cells respond than did naive B cells in the primary response