contortus have reported cellular infiltrations in the mucosa and regional lymph nodes, increases in T CD4+, T CD8+, T gamma delta ([gamma][delta]) and B lymphocytes, eosinophils and mastocytes [5, 11, 17, 75].
The hyperplasia of mastocytes in the abomasum mucosa is associated mainly with the presence of adult parasites and is greater in re-infections [10, 42], requiring a continuous stimulation on the part of parasitic antigens [4, 10].
Negative correlations have been registered between the values of EPG and mastocytes  and between these cells and the parasitic burden .
Activation of TLRs triggers a cascade of intracellular events leading to activation of several transcription factors, including NF-[kappa]B, activator protein1 (AP-1), and IFN-regulatory factor-3 (IRF-3) and -7 that regulate the expression of various cytokines and chemokines, responses that are performed in the CNS mainly by mastocytes and microglia.
In the adult brain, mastocytes are mainly found in leptomeninges  and thalamus close to the BBB [26, 27], but they are also present early in brain ontogeny [28, 29].
Murine mastocytes express the mRNA of TLRs 1-4 and 6-9 but not TLR5 [32-36].
The AD patients have a distorted, hyper acute response to stress, based on the activation of the Th2 cells and mastocytes
, the dysfunction of the HPA and NNA and as a consequence, of the release and expression of neurogenic cutaneous inflammation mediators.
IgE can bind to eosinophils, mastocytes
, and macrophages, turning them into potent antitumor cells [102,116,117].
It is known that activated mastocytes
contribute to higher expression of mRNA for IL-31 receptors [2, 3].
Nociceptors that respond to acetic acid depend on the release of some cytokines, such as TNF, IL-1, and IL-8, from macrophages and mastocytes in the peritoneal cavity [15-17].
The pain induced by CFA causes the activation or release of various endogenous inflammatory mediators, such as histamine, serotonin, and kinins, through the degranulation of resident mastocytes, in addition to an increase in prostaglandins caused by the activation of cyclooxygenases and cytokines, such as IL-1[beta] and TNF, that stimulate nociceptors [16,18, 24-26].
Although tumor-associated macrophages (TAM's) constitute the principal source of MMP9 in the zone of neoplastic growth, it should be noted that this molecule may be also synthesized by neoplastic cells, stromal neutrophils, fibroblasts, and mastocytes