The initial encounter of a naïve immune-competent lymphocyte with an antigen induces a primary immune response; a later contact of the host with the same antigen will induce a more rapid and heightened secondary immune response.
The amplified population of memory cells accounts for the rapidity and intensity that distinguishes a secondary response from the primary response.
We apply the concept of immune response to produce needed immunity in a host through vaccination. Antigens administered in the body via vaccination imitate the infectious agent thus body produces T-lymphocyte, B-lymphocyte, and antibodies against it. If a vaccinated person encounters infection later in life (by the same pathogen), the memory B cells and T cells, fight off the infection, rapidly, and in heightened response thus giving needed protection.
In some vaccines, the first dose (primary response) does not provide needed immunity and that immunity may begin to wear off after a certain period, in such cases we provide more shots and even booster dose to keep immunity at the needed level (i.e. to maintain the population of memory cells).
Major characteristics/differences between primary and secondary immune response is summarized in this table:
|Primary Immune Response||Secondary Immune Response|
|Definition||Immune response against primary antigenic challenge||Immune response against subsequent antigenic challenge|
|Response||Low, sluggish (appear late) and short lived||Prompt, powerful and prolonged (long lasting)
|Antibody producing cells||Naïve B cells||Memory B cells|
|Antibody levels||Antibody levels peak in the primary response at about day 14 and then begin to drop off as the plasma cells begin to die.||Because there are many more memory cells than there were naïve B cells for the primary response, more plasma cells are generated in the secondary response, and antibody levels are consequently 100 to 1000 fold higher.|
|Lag period||Lag period in longer (4-7 days)|
This lag is the time required for activation of naive B cells by antigen and TH cells and for the subsequent proliferation and differentiation of the activated B cells into plasma cells.
|Lag period is absent or short (1-3 days)
The secondary response reflects the activity of the clonally expanded population of memory B cells. These memory B cells respond to antigen more rapidly than naïve B cells.
|Negative phase||No negative phase||Negative phase may occur|
|Antibody Isotype||Antibody produced in low titer and is of IgM type. |
In the disease diagnosis presence of IgM is suggestive of recent primary infection.
|Antibody produced in high titer and mainly is of IgG type (IgA or IgE in certain situations). In the diagnostics, presence of IgG should be interpreted cautiously as it may be because of previous vaccination, subsequent sub-clinical infections (local cut-off titre, or previous infections with the same agent).|
|Specificity of Antibody||Antibodies are more specific but less avid||Antibodies are less specific but more avid|
|Antibody Affinity||Lower average affinity, more variable
|Higher average affinity (affinity maturation)|
|Induced by||All immunogens (Both T dependent and T independent antigens are processed by primary immune response)||Only protein antigens |
(Only T dependent antigens are processed)
Nisha RijalI am working as Microbiologist in National Public Health Laboratory (NPHL), government national reference laboratory under the Department of health services (DoHS), Nepal. Key areas of my work lies in Bacteriology, especially in Antimicrobial resistance.
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