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histocompatibility testing 328 Histoplasma immunity
Class II MHC molecules are glycoprotein histocompatibility antigens
that play a critical role in immune system cellular interactions. Each
class II MHC molecule is comprised of a 32- to 34-kDa α chain and a
29- to 32-kDa β chain, each of which possesses N-linked oligosaccharide
groups, amino termini that are extracellular, and carboxyl termini that are
intracellular. Approximately 70% of both α and β chains are extracellular.
MHC class II molecular structure.
mice, across which incompatible grafts are rejected within
1 to 2 weeks, and several minor histocompatibility loci with
more subtle antigenic differences, across which only slow,
low-level graft rejection reactions occur.
histocompatibility testing
Determination of the major histocompatibility complex
(MHC) class I and class II tissue types of both donor and
recipient prior to organ or tissue transplantation. In humans,
HLA-A, HLA-B, and HLA-DR types are determined, followed
by cross matching donor lymphocytes with recipient
serum prior to transplantation. A mixed lymphocyte culture
(MLC) is necessary for bone marrow transplantation, in
conjunction with molecular DNA typing. The MLC may
also be requested in living related organ transplants. As in
renal allotransplantation, serum samples of organ recipients
are tested for percent reactive antibodies, which reveals
whether they have been presensitized against HLA antigens
of organs for which they may be the recipients.
histone antibodies
Antibodies of the immunoglobulin G (IgG) class against H2A–
H2B histones detectable in essentially all procainamide-induced
lupus patients manifesting symptoms. They are also present in
approximately one fifth of systemic lupus erythematosus (SLE)
patients and in procainamide-treated persons who do not manifest
symptoms. Antibodies against H2A, H2B, and H2A–H2B
complex react well with histone fragments resistant to trypsin.
By contrast, antibodies in the sera of SLE patients manifest reactivity
for intact histones but not with their fragments. In lupus
induced by hydralazine, antihistone antibodies react mainly with
H3 and H4 and their fragments that are resistant to trypsin.
histone autoantibodies ((non-H2A–H2B)–DNA)
H1–H4 autoantibodies of the immunoglobulin M (IgM) isotype
are broadly reactive and frequently found in patients with systemic
lupus erythematosus (SLE) and in normal persons taking
various medications. Patients with localized scleroderma (40 to
60%) and those with generalized morphea (80%) demonstrate
autoantibodies against histones H1, H2A, and H2B. Systemic
sclerosis patients (29%) and diffuse cutaneous systemic sclerosis
patients (44%) reveal histone H1 autoantibodies associated
with the severity of pulmonary fibrosis in systemic sclerosis.
Autoantibodies against histone (H2A–H2B)–DNA complexes
are seen more frequently in scleroderma-related disorders than
in SLE. Elevated IgA antibodies against all H1, H2A, H2B, H3,
and H4 are detectable in IgA nephropathy, primary glomerulonephritis,
membranous glomerulonephritis, and idiopathic
nephrotic syndrome. The serum histone autoantibody titer
is also positively correlated with the extent of dementia in
Alzheimer’s disease.
histone (H2A–H2B)–DNA complex autoantibodies
Immunoglobulin G (IgG) autoantibodies against histones
develop in drug-induced lupus (DIL) in the absence of
other autoantibodies. They show high reactivity with histone
H2A–H2B dimers, when induced by procainamide.
The autoantibodies diminish when the drug is discontinued.
IgM autoantibodies against histone H1–H4 are found
frequently in systemic lupus erythematosus (SLE) and in
persons receiving a variety of medications. Autoantibodies
against histone (H2A–H2B)–DNA complexes are generated
in DIL attributable to procainamide, quinidine, acebutolol,
penicillamine, and isoniazid but not methyldopa.
H2A and H2B histone linear epitopes are identified by
separate histone autoantibody populations associated with
SLE, DIL, juvenile rheumatoid arthritis, and scleroderma.
Histoplasma immunity
Cell-mediated immunity is the main host defense against
infection with Histoplasma capsulatum. The specific cell-