Biology Reference
In-Depth Information
lymphocytic choriomeningitis virus, but with altered T-cell receptor (TCR) reper-
toires, and they became functional memory cells capable of recall responses
[96]
.
Current evidence implicates HP in autoimmune diseases and transplant rejection,
and suggests that it may represent a barrier to tolerance in protocols that use T-cell
depletion
[97]
.
Clonal competition is a component of homeostasis that may contribute to selec-
tion of the peripheral T-cell repertoire
[98]
. Tregs play a major role in the control of
HP
[99]
. HP memory CD8() T cells controlled bacterial infection as effectively as
“true” memory CD8() T cells, but their protective capacity required the presence
of CD4() T cells during HP. The necessity for CD4 help was overcome, however,
if the HP memory CD8() T cells lacked expression of TRAIL (tumor necrosis fac-
tor-related apoptosis-inducing ligand; also called Apo-2L). Thus, like conventional
CD8() memory T cells, the protective function of HP memory CD8() T cells
shows dependence on CD4() T-cell help
[100]
.
Similar factors are required for production of protective memory CD8 T cells via
both homeostatic and conventional pathways. Induction of protective HP memory
CD8 T cells requires CD4() T-cell “help,” which we show is antigen nonspecific
yet requires CD40L-CD40 interactions with host cells. The functional competence of
HP memory CD8 T cells also requires release of endogenous bacterial components
(which follows irradiation-induced lymphopenia), potentially mimicking the role
of adjuvants in conventional immune responses. Lymphopenic environments lack-
ing these key factors support similar CD8 T-cell HP and the acquisition of memory
phenotype, yet the HP memory cells generated are defective in pathogen elimination
[101]
. HP memory T cells provide protection without compromising the true-memory
population. Differences in HP and true-memory T cells may reveal the basis of com-
petition for limited resources within the memory T-cell compartment
[102]
.
The significance of this phenomenon is that memory T lymphocytes are able to sur-
vive major disasters and bring back immune function once the crisis is over. During
APR, the ADIM system is suppressed by Tsrs and GCs, but not destroyed. The possibil-
ity of recovery is present and ADIM function recovers after acute illness. We proposed
that healing is under hypothalamic regulation, with VP as the principal regulator
[28]
.
1.5 Autonomy and Redundancy
Immune reactions may be induced
in vitro
, which argues for the autonomy of
immune function. Indeed, the fully differentiated cells of the INIM system can
function under diverse conditions with little regulatory input from the host. When
it comes to adaptive immunity, the primary response is dependent on pituitary hor-
mones that must be provided. However, the secondary response could develop in the
absence of such hormones because memory cells survive hypophysectomy
[38]
.
GH, PRL, erythropoietin, thrombopoietin, and leptin all have structures similar
to type I CTKs, and their receptors also belong to the same receptor superfam-
ily. Short-chain type I CTKs include IL-2, -3, -4, and -5; granulocyte macrophage
