It has been demonstrated that there are two distinct mast cell phenotypes based on
their biochemical properties:
n Mucosal mast cells which are normally only found in the gut mucosa and contain mast
cell protease II.
n Connective tissue mast cells which are present in most tissues of the body outside of
the alimentary canal and contain mast cell protease I.This separation has now been shown to be not quite so simple, both types of mast cells
having been shown to be present in the livers of rats infected with tapeworm metaces-
todes and in connective tissue hyperplasia caused by the infection.
Mast cells have often been linked with the expulsion of gut parasites but the results
of numerous investigations into this phenomenon have still not yet demonstrated con-
vincingly whether or not mast cells are the prime factors in the expulsion process.
A case has been made for mast cells damaging both the worms and gut tissue in mice
infected with H. diminuta.
One of the properties of mast cells is the secretion of angiogenic factors. This results
in an increase in the growth of capillaries and blood flow to the infected area. Histamine
and other compounds derived from mast cells affect the permeability of the walls of
endothelial cells. This allows for a leakage of fluid into the infected zone and the accu-
mulation of muco-polysaccharide compounds, eg glycosaminoglycans (GAG). This
creates a semi-viscous environment for the parasite to inhabit. All the nutrients that
the parasite requires are probably in solution within the GAG. Hence it may just be
that the parasite has become adapted to the host’s response and actually uses it to its own
advantage.
n 5.7 THE SECOND PHASE OF THE IMMUNE RESPONSE
There are only a few diseases caused by the types of parasite already outlined that result
in the death of the host. That is there are very few parasites that can be considered to be
‘killers’ like the pathological bacteria and viruses. The phagocytic cells are activated
by the presence of a parasite and if they engulf part of or all the parasite they become
antigen-presenting cells (APCs).
The presence of activated APCs and cytokines stimulates the T lymphoyctes and in
particular the T helper cells. In order for an adaptive immune response to begin both the
T cells and B cells have to react to an antigen peptide associated with MHC class II
molecules. Both T cells and B cells have antigen receptors on their cell membranes:
T cell antigen receptor (TCR) and surface immunoglobulin (sIg) respectively.
Activation of mature T cells leads to the expression of surface molecules. Only those
T cells which express receptors that react to non-self antigen in the presence of an MHC
molecule are selected. Immature T cells that do not express receptors reacting to self-
antigen are eliminated (by clonal selection). The interaction between an antigen peptide
associated with an MHC molecule on antigen-presenting cells (APCs) requires addi-
tional signals (co-stimulatory signals) provided by co-stimulatory molecules.
The co-stimulatory molecules are thought to have evolved from PAMPs (pathogen asso-
ciated molecular patterns) on the pathogen and PRRs (pathogen receptor regions) on the
host phagocytic cell (see section 5.1). The primary recognition of the pathogen is non-
specific for cells already present that have not been specifically cloned to recognise the
pathogen. The contact between co-stimulatory molecules stimulates the production of
the cytokine IL-2 which then initiates the beginning of an adaptive immune response.
INTRODUCTION TO HOST RESPONSE