In article <p_travers-0906951440420001 at macmhc.cryst.bbk.ac.uk>,
Paul J Travers <p_travers at icrf.icnet.uk> wrote:
>>Ephraim,
>> I suspect your statement is a little too general. How do you
>account for the observation that inherited deficiencies in late (ie lytic
>pathway) complement components are specifically associated with
>susceptibility to Neisseria infections (a gram- organism). In these cases
>the early complement components are intact and capable of acting as
>opsonins, but this is insufficient to control this particular group of
>pathogens.
>> As to whether in general adaptive immune responses are associated
>with resistance to gram- bacteria, isn't there a window of susceptibilty
>in infants whose onset correlates with the disappearance of maternal
>immunoglobulin and which decays as the infants own immunoglobulin levels
>rise? Does this not suggest that antibody (which I would class as part of
>the adaptive immune system) plays a role in host defence against gram-
>pathogens?
>Paul,
I would agree with your above argument but I think that the Ig plays an
intersting dual role in the adaptive immune response. Some B-cells can
produce Ig in a T-independent fashion. However these B-cells appear to
rearrange a more restricted set of V-genes and do not undergo somatic
hypermutation to a detectable extent. However it is highly likely that
the Ig from thse B-cells plays a role in immune complex formation with
antigen and hence in antigen presentation by FcR and CR bearing cells.
Obviously to some extent the repertoire of these B-cells depends upon
the genetic inheritance of the V-gene segments.
So the question I find myself asking is how important is the T independent
B-cell response in getting the whole adaptive immune response primed in
the first place?
