Question

You have joined a research lab that is testing new vaccines for a new strain of the influenza A virus (IAV). The lab's prior studies have shown that when C57BL/6 laboratory mice are given non-pathogenic bacteria that have been engineered to express a 16 amino acid peptide, after about a month the mice produce IgG antibodies that effectively neutralize IAV. Your project is to test serum samples from healthy adult humans who were given these bacteria 6 weeks ago as part of a pilot clinical trial. You find that you can clearly detect IgG antibodies against IAV from about a third of the samples, but cannot detect IAV-specific antibodies from the remainder of the samples. Which of the following is the most likely characteristic shared by individuals who produced a detectable antibody response?

Group of answer choices:

A. They have a genetic polymorphism that causes their T cells to produce comparatively high amounts of IL-2

B. They are people who also have pollen allergies

C. They all have genetic polymorphisms in genes for complement proteins that result in inefficient clearance of bacteria by the membrane attack complex (MAC)

D. They express MHC class II allotypes that bind efficiently to the 16 amino acid peptide expressed by the bacteria

E. They express a self protein that contains an amino acid sequence identical to the 16 amino acid peptide expressed by the bacteria

Answer 1

Option D, it seems to correct answer

D. They express MHC class II allotypes that bind efficiently to the 16 amino acid peptide expressed by the bacteria.

After entry of bacteria as a vaccine some individal produced IgG while some did not. It is due to variation in MHC II haplotype. MHC II is present on APC cell ( antigen presenting cells) which shows antigen to Th cell and cause activation of both B and T cell. Activated T cell , release IL 2. So due to the variation in MHC II haplotype, some of the individuals APC process the peptide while some did not. Person we processed showed IL2 production, person who did not processed peptide did not produced IL 2