1. Secondary Immune Response
- Purvi Gosrani

2. Introduction
A 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

4. 1°ImmuneResponse
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°ImmuneResponse
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).

5. Immunological MemoryIs Sustained ByClones Of Long Lived
Memory T Cells And B Cells
After 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

7. Vaccination Against A Pathogen Can Generate Immunological Memory
That Persists For Life
The 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

8. Pathogen–Specific MemoryB CellsAre More Abundant And Make Better
Antibodies Than Do Naive B Cells
In 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