From: Billi Goldberg <bigoldberg@igc.apc.org>
Subject: Revised DNCB Fact Sheet
Note: Copyright 1992, Dan R. Greening. Non-commercial reproduction allowed.
Archive-Number: 6055
Organization: unspecified
Date: Wed, 2 Sep 92 18:11:12 PDT

                               DNCB FACT SHEET
                              by Billi Goldberg

PURPOSE 
DNCB is a potent contact sensitizer and an alternative treatment for human 
immunodeficiency virus (HIV) infection and acquired immune deficiency syndrome 
(AIDS).

INFORMATION
Additional information concerning DNCB can be obtained from DNCB Treatment 
Issues, 2261 Market Street #436, San Francisco, CA 94114. DNCB artwork and 
label procurement resources are available on request

CHEMICAL NAME
1-chloro-2,4-dinitrobenzene (C6H3ClN2O4)

AVAILABILITY 
Prepared kits and single vials are available for direct sale or mail order, 
with standardized treatment instructions, from the Healing Alternatives 
Foundation (HAF), 1748 Market St., San Francisco, CA 94114, (415) 626-2316. 
Starter kits cost about $20.00 which includes a voluntary contribution to HAF; 
single vials cost $1.65; and kits will be furnished without cost if necessary. 
Instructions were written by a dermatologist from UCSF and have been updated 
based on usage information. 

HAF does not endorse any HIV/AIDS treatment and only provides access to 
alternative therapy information and products.

MANUFACTURE 
Produced in solvent or crystal form by a number of chemical companies in 
several countries. It can only be ordered for human use in the USA by 
authorized medical doctors or researchers. For industrial or business 
purposes, it can be obtained by the company representative using its resale 
number. An example of this would be a company involved in color photography 
which would order the DNCB from Eastman Kodak Company.

PROCUREMENT 
Sigma Chemical Company
In the USA/Canada DNCB can be ordered in crystal form from SIGMA Chemical 
Company, P.O. Box 14508, St. Louis, MO 63178-9916; phone 800-325-3010; fax 
800-325-5052. Outside USA/Canada, call collect to 314-771-5750; fax 314-771-
5757. 

Using the 1992 SIGMA Catalog as reference: Order only the 99% purity crystals 
which are light brown to yellow in color. Catalog number is C 6396; cost is 5 
grams for $11.05, 100 grams for $11.75, and 500 grams for $32.20; all prices 
FOB Sigma.

Eastman Kodak Company
DNCB can be ordered in crystal form from Eastman Kodak Company by calling 1-
800-225-5352, press one(1) for chemical supplies in non-bulk; for bulk 
chemical supplies in 1 kilogram or greater, press two(2). 

The latest procurement information from Eastman Kodak Company is catalog 
number #1018860 for 100 grams at $29.00; catalog number #1019009 for 500 grams 
at $91.70. The purity of this product is 98% which is appropriate.

CONTAINERS
California Glass Company
The appropriate containers and caps for DNCB can be obtained from the 
California Glass Company, 155-98th Avenue, Oakland, CA, phone is 510-635-7700. 
The bottles are amber colored, 5 dram in size, order number #03000040 and cost 
$29.60 per case of 144 bottles. The white caps that come with the bottles must 
be disposed of as they are not air tight and the acetone will evaporate. Order 
only the 24mm black molded polyseal caps #08017000 which cost $155.79 per 1000 
caps.

STATUS 
DNCB is not approved for manufacture as a drug or as a treatment for HIV/AIDS. 
It is occasionally applied as topical treatment for refractory warts and 
alopecia areata (hair loss) and has been used successfully in humans as a 
treatment for malignant melanoma, and as immunotherapy for skin lesions.

USAGE 
DNCB is to be applied only topically (externally) using treatment instructions 
provided with the solution. It is not to be used internally. If the treatment 
instructions are followed, DNCB has not shown toxicity at recommended 
application/dosage. Contact dermatitis can result if too much solution is used 
or at a greater than recommended frequency. Evaporation of the acetone will 
cause the percentage of DNCB in the solution to increase resulting in severe 
blistering, reddening, and itching. If in doubt, discard old solution and 
replace with new solution.

PREPARATION 
10% SOLUTION:   Dissolve 12 grams of DNCB crystals in 1/4 cup of acetone.
2% SOLUTION:    Dissolve 2.4 grams of DNCB crystals in 1/4 cup of acetone.
0.2% SOLUTION:  Dissolve 0.24 grams of DNCB crystals on 1/4 cup of acetone.
0.02% SOLUTION: Dissolve 0.024 grams of DNCB crystals in 1/4 cup of acetone.

Use only glass containers and stirring rods to eliminate reactions between 
DNCB solution and plastic or metal implements. To prevent evaporation of the 
solution resulting in an unacceptable solution strength: (1) seal the solution 
in small amber bottles using special leak-proof caps, (2) refrigerate 
containers, and (3) replace solution after six months.

When preparing the DNCB crystal-acetone solution, be careful, use rubber 
gloves, and avoid contact with the solution. Use a large pipet and a pipet 
helper to fill bottles from the solution containers. A liquid handling bottle-
top dispenser is also suitable for filling bottles as is a dispenser with a 
petcock such as used in large volume wine containers. Various liquid handling 
materials can be ordered the Sigma Chemical Company catalog.

CONTACT SENSITIVITY
When chemically reactive compounds are applied directly to the skin, they 
result in systemic sensitization to various metabolites of the sensitizing 
compound. This is known as a Delayed Type Hypersensitivity Type IV which is a 
cell mediated immune reaction. Sensitizing agents such as DNCB probably form 
dinitrophenylprotein complex with various skin proteins resulting in a 
conjugate that is immunogenic. DNCB does not have the capacity to cause 
respiratory sensitization. The ability of a subject to develop contact 
sensitivity to new antigens such as DNCB is a measure of cellular immunity.

Antigens such as DNCB, urushiol of poison ivy and diphencyprone are potent 
antigens and can sensitize most subjects (that have not had prior exposure) 
when applied to the skin. Oral administration of a contact sensitizer such as 
DNCB results in tolerance to the sensitizer when it is applied cutaneously (on 
the skin). 

Many other substances such as organic compounds (lipoproteins, 
lipopolysaccharides, etc.), inorganic salts of metals, drugs, and metal 
allergens such as nickel, cobalt, chromium, zinc, copper, mercury, tin, gold, 
iron, and germanium can act as immune boosters when conjugated (become 
immunogenic) by initiating delayed type hypersensitivity reactions (DTH). 
These substances can be administered by internal or external methods. The four 
types of DTH are IgE-mediated (Type I), cytotoxic-antibody-mediated (Type II), 
immune-complex-mediated (Type III), and T effector cell-mediated (Type IV). 
Individuals can be classified as either responders or non-responders to 
various immunogenic substances depending on individual tolerance. 

ACTION
DNCB or contact sensitization is a method of immunopotentiation. 
Immunopotentiation is a process which directly enhances one or more specific 
immune functions, or modifies one or more components of the complex 
immunoregulatory network to achieve its effects through indirect mechanisms.

The mechanism of biological action of DNCB is due to Delayed Type 
Hypersensitivity (DTH) Type IV which involves the initiation of the Th1 or 
cell mediated immune response (CMI). The DTH response is initiated by DNCB 
application which is a potent initiator of contact sensitivity in 
approximately 98% of individuals. The humoral or antibody system is not 
activated or involved in DTH Type IV. The primary infections in AIDS are of an 
intracellular nature which can only be controlled by the cell mediated immune 
response; the antibody system is ineffective in controlling these microbial 
agents. 

Excess sunlight or ultra violet radiation will result in immunodepression 
compromising the delayed type hypersensitivity reaction. When using DNCB, 
avoid excess sun or UV irradiation; this includes tanning salons.

Scientists and researchers have known for years that immunological adjuvants 
added to vaccines will stimulate an earlier, stronger, or more prolonged 
response to an antigen thus augmenting specific immunity to the vaccine. The 
specific adjuvant can be selected,  according to its immunogenicity, to 
initiate humoral or cellular immune responses depending on which is involved 
in acquired immunity towards the vaccine microbial pathogen. Generally, oral 
vaccines initiate cellular responses (e.g. Sabin polio vaccine) while 
parenteral administered vaccines initiate humoral responses. The adjuvants are 
presented by antigen presenting cells to memory T lymphocytes thus augmenting 
the self-perpetuating effector cell response resulting in increased 
immunological memory against weak immunogenic vaccine antigens. It is 
interesting to consider why the concept of adjuvants, which is similar to the 
action of DNCB, was not considered as a treatment for AIDS when it has been 
known for years that the primary microbial pathogens involved in AIDS are of 
the intracellular variety.

TREATMENT
DNCB applications consists of saturating a cotton swab (Q tip) with the 
appropriate solution and applying to the application site which should be at 
least 2 inches in diameter. Repeat this procedure a second time. Do not over 
apply the solution, twice is enough.

The sensitizing 10% DNCB solution is applied on the underside of the lower 
forearm or the inside of the upper arm. One month later (never less than one 
month), verify sensitization by applying the 2% solution to the opposite arm. 
It takes at least one month for the DNCB memory T lymphocytes to form and 
circulate throughout the body. Within 24 to 72 hours, the site of the 10% 
initial application should react (reflare) with a slight to moderate 
reddening, itching, or burning. If this happens, the individual is sensitized 
to DNCB and weekly applications of 2%, 0.2%, or 0.02% (whichever is 
appropriate) can commence with each application at a different site. If the 
application results in a slight to moderate reddening, itching or burning at 
the application site, the solution strength is appropriate. If blistering or 
weeping occurs, use a lesser strength solution. If there is no response, use a 
greater strength solution for the next weekly application.

If there is no reflare, continue using the 10% solution weekly until a reflare 
at any previous application site occurs. Sensitization is incremental; each 
10% application adds to the previous one thus increasing prospects of complete 
sensitization. This technique should result in sensitization regardless of 
immunodepression. The DNCB hapten has a long half-life therefore the reflare 
results from the immune system attacking the DNCB hapten at the site of last 
application with the 10% solution. Weekly applications should start, as stated 
above, after the reflare.

A collaborative relationship with your doctor or dermatologist is recommended 
when using DNCB. But, under no conditions or recommendations, deviate from the 
DNCB Treatment Instructions unless a knowledgeable dermatologist, experienced 
in DNCB use and contact sensitization, makes the recommendation. Well-meaning 
but ill-informed medical personnel have suggested that the initial application 
be less than 10%. This is totally inappropriate and undermines the basic 
concepts of sensitization, verification and treatment with DNCB.

OPPORTUNISTIC INFECTIONS
DNCB does not replace approved treatment/prophylaxis for opportunistic 
infections. One should not discontinue prescribed treatment/prophylaxis for 
opportunistic infections when utilizing DNCB. It is especially important that 
prophylaxis/treatment for Pneumocystis carinii pneumonia (PCP) be considered 
or continued if prescribed by a doctor. It has been shown, anecdotally, that 
DNCB will control opportunistic infections BUT THIS HAS NOT BEEN PROVEN.

DISCUSSION 
On first application of the 10% DNCB solution, a primary immune response is 
initiated. DNCB is a hapten which means that it is antigenic but cannot 
initiate an immune response alone (it is not immunogenic). As the DNCB hapten 
migrates from the dermis, it attaches to a protein; this is known as a hapten-
protein conjugate which is now immunogenic since a peptide is involved. 
Langerhans cells in the epidermis will migrate from the epidermis, process the 
conjugate, differentiate into veiled dendritic cells, utilize the lymphatic 
circulation, and then proceed to the draining lymph nodes where they become 
interdigitating dendritic cells. 

The processed DNCB antigen will then be presented to naive CD4 T lymphocytes 
(CD45RA molecule). It is surmised that the DNCB conjugate, when involved in 
antigenic competition, is a superior antigen. During the antigenic 
presentation to T lymphocytes, the T cells change from quiescent (G0 phase) 
cells to active lymphoblast transformed (G1 phase) cells. After appropriate 
cytokine signaling (stimulatory and co-stimulatory), the helper CD4 T 
lymphocytes will be activated (S phase) and will proliferate forming 
immunological memory CD4 T lymphocytes (CD45RO molecule) and additional helper 
CD4 T lymphocytes . A reaction or immune response will then take place at the 
site of initial application involving redness and itching. 

After one month, verification is obtained by applying the 2% solution at a 
different site. If within 24 to 72 hours, the initial site reflares (blushing 
or reddening), sensitization has been obtained and weekly treatment 
applications are applied. Use the solution strength for weekly treatments that 
results only in reddening and itching (if blistering or weeping occurs, use a 
lesser strength solution). If there is no reflare, continue using the 10% 
solution until reflaring occurs at one of the previous application sites. 
Complete sensitization is incremental therefore, sooner or later, almost 
everybody will sensitize.

The weekly doses result in a secondary immune response in the lymph nodes 
which activates the immunological memory resulting in a quicker and more 
efficient cell mediated immune response. This response results in a systemic 
activation of effector cells such as cytotoxic T lymphocytes, natural killer 
cells (form of lymphocyte) and monocytes/macrophages (monocytes become 
macrophages when they leave the peripheral blood) which will eliminate the 
DNCB hapten. 

Monocytes/macrophages (mononuclear phagocytes) are infected with many viruses 
including adenoviruses, herpesviruses (herpes simplex, cytomegalovirus), 
retroviruses (HIV), and other intracellular microbial pathogens involved in 
AIDS opportunistic infections (OIs) such as bacteria (chlamydia, mycobacteria, 
salmonella), fungi (aspergillus, blastomyces, candida, cryptococcus, 
histoplasma), and protozoa (leishmania, toxoplasma). Most of the opportunistic 
infections in AIDS affect primarily the mucosa associated lymphoid tissues 
(MALT) and can only be controlled by the cell mediated immune response (the 
humoral or antibody system is ineffective against these intracellular 
pathogens). 

Since the peripheral blood monocytes and tissue macrophages circulate 
throughout the body, they are considered the vehicle that causes the systemic 
spread of HIV and dissemination of OIs. Some of the various types of 
macrophages are Kupffer cells (liver), alveolar macrophages (lung), 
histiocytes (connective tissues), red pulp macrophages (spleen), osteoclasts 
(bone), type A cells (synovium) and microglia (central nervous system 
including brain). 

Activation and priming of macrophages result not only in the internalization 
(endocytosis) and breakdown of microbial pathogens (phagocytosis) but antigen 
preparation (proteolysis) and presentation (on Class I MHC and Class II MHC 
molecules) of the pathogens to the TCR:CD3 receptors (molecules) of the memory 
CD4 and CD8 T lymphocytes. The CD4 and CD8 molecules on the T lymphocytes are 
adhesion molecules and may be involved in signal transduction. 
Langerhans/dendritic cells in the lymphoid tissues are potent antigen 
presenting cells, have Class I and II MHC (major histocompatibility complex), 
and can also present antigens to memory CD8 and CD4 T lymphocytes. 

Almost all cells have Class I MHC while antigen presenting cells (APC) also 
have Class II MHC. Langerhans, dendritic and B cells constitutively express 
Class II MHC; mononuclear phagocytes are weak expressors which is increased by 
IFN-gamma; endothelial, fibroblasts, stromal and some epithelial cells are 
negative expressors which is induced by IFN-gamma; and T lymphocytes express 
Class II MHC upon activation. Therefore, during an immune response which 
increases the production of the cytokine IFN-gamma, additional cells are 
capable of antigen presentation resulting in increased immune responses and 
increased clearance of microbial pathogens in the blood and lymph vessels 
(endothelial cells) and tissue system. CD8 T lymphocytes only recognize 
antigen in conjunction with Class I MHC molecules (HLA-A, HLA-B, HLA-C in 
humans); CD4 T lymphocytes only recognize antigen in conjunction with Class II 
MHC (HLA-DP, HLA-DQ, HLA-DR in humans) molecules.

The result of this immune system interaction will be new cell mediated immune 
responses which will initiate proliferation of helper CD4 T lymphocytes and 
cytotoxic CD8 T lymphocytes, increase the memory T lymphocyte pool, and 
activate effector cells to eliminate the pathogens.

It is also interesting to note that malignant tumors express a variety of 
antigens that may stimulate and serve as targets for anti-tumor immunity. The 
major effector cells of anti-tumor immunity are most likely natural killer 
cells, cytotoxic T lymphocytes and macrophages. These effector cells are 
activated by the cell mediated immune response initiated by delayed type 
hypersensitivity. It has not been convincingly demonstrated (but it is 
assumed) that natural or acquired immunity in vivo  can control the 
development and growth of malignant tumors. It is known, however, that AIDS 
immunodepressed individuals have a greater susceptibility to malignant tumors 
during disease progression. This leads to the distinct possibility that 
natural or acquired immunity has been immunosuppressed by microbial pathogens 
and that hyperimmune activation may initiate an anti-tumor effector cell 
response.

The memory T lymphocytes (CD45RO molecule) already exist since the microbial 
pathogens in AIDS are pre-existing infections (previously acquired immunity), 
therefore the result is a secondary immune response. Cytotoxic T lymphocytes, 
natural killer cells (NK) and macrophages will be activated resulting in 
elimination of more pathogens ad infinitum. Macrophages and NK cells are not 
memory specific (as are helper and cytotoxic T lymphocytes) and will randomly 
present and eliminate non-self microbial pathogens. These actions result in 
self-perpetuating immune responses which will continue until suppressed by 
suppressor T lymphocytes that have been activated by the weekly DNCB 
application or the additional immune responses. 

The "self-perpetuating immune responses" could involve "bystander effects." 
These effects are defined as the result of cellular interactions that occur 
without antigen recognition or under conditions where antigen and receptors 
for antigen are not involved. Specific T cell  proliferative responses are 
elicited by specific antigens on antigen presenting cells which are recognized 
by the T cell antigen receptor (TCR:CD3 complex).  This proliferative response 
can also affect T lymphocytes in the vicinity of the response with unrelated T 
cell receptors. Proliferation of these bystander T cells occur independently 
but simultaneously with antigen specific T cell responses. Cytotoxic T 
lymphocytes (CTL) are effector cells that specifically kill target cells 
bearing an appropriate antigen recognized by their receptor (TCR:CD3 complex). 
It has been noted that during this specific killing, nonspecific lysis of 
unrelated bystander target cells takes place. The unrelated cells do not 
present the appropriate antigen and are not recognized by the CTL receptor.  

The bystander effects might be caused by lymphokine secretions during 
activation of T lymphocytes that act in a nonantigen specific way on other 
cells present at the site of the immune response; these cells could then be 
recruited into the overall immune response. The types of cells involved could 
be T or B lymphocytes, macrophages, Langerhans/dendritic cells and  target 
cells for CTL, lysis or phagocytosis. 

It has been shown in studies that contact sensitization causes all the 
Langerhans and dendritic cells (not just where the DNCB was applied) to 
migrate from the mucosa membranes (MALT) as veiled dendritic cells (VDC) to 
the lymph nodes (draining, contralateral and distant) where they become 
interdigitating dendritic cells (IDC). These cells will then be destroyed 
(probably in the lymphoid organs) and replaced by the immune system at their 
original locations where migration commenced. This action is extremely 
important since the most recent research has shown that Langerhans  and 
dendritic cells (LC/DC) are infected and/or dysfunctional due to HIV. By 
eliminating and replacing these compromised cells, antigen presenting 
capability is restored. Dendritic cells are considered the most potent and 
efficient antigen presenting cells in the immune system.

A new research focus in HIV/AIDS has hypothesized that Langerhans/dendritic 
cells (LC/DC), which are either infected by HIV or have HIV on their dendritic 
processes, can contaminate memory T lymphocytes that they come in contact with 
while presenting antigens in the lymphoid organs (lymph nodes, PeyerUs 
patches) or lymphoid tissues. This could result in the infection and deletion 
of the CD4 T lymphocytes. It has also been surmised that LC/DC are rendered 
dysfunctional by HIV. They then become ineffectual in antigen presentation 
capabilities and/or lack mandatory costimulatory signals resulting in clonal 
deletion or clonal anergy of the memory CD4 T lymphocytes for HIV or other 
microbial pathogens involved in AIDS. (This ineffectual antigen presentation 
in the absence of costimulation can be bypassed if the immune system is 
activated at the time of antigen administration by an immunostimulant.) This 
pronounced  memory CD4 T lymphocyte loss results in uncontrollable microbial 
replication of opportunistic pathogens which accelerates disease progression 
and causes death. 

Follicular dendritic cells (FDC) in the lymphoid organs are considered a 
repository of HIV. These cells are long-living (up to twenty years) and are 
part of a specialized network (e.g. lymph nodes) that brings together antigen, 
APCs, B cells, and helper T lymphocytes. Cell-free HIV or HIV immune complexes 
reside (bead) on the elongated dendritic processes of FDC and can infect 
memory CD4 T lymphocytes and other susceptible cells that come in contact with 
these processes. FDC are not antigen presenting cells per se  but viral 
particles from the processes can be acquired by B cells (which are APCs for 
antibody production) and result in HIV antibody proliferation. 

Dendritic cells that migrate to the lymphoid organs for antigen presentation 
of the DNCB conjugate to memory CD4 T lymphocytes will initiate immune 
responses and activate effector cells. Activated tissue macrophages, and 
natural killer cells could then destroy the HIV or HIV immune complexes in the 
lymphoid organs or activate additional immune responses specific for HIV 
triggered by macrophage antigen presentation. Pathological studies of lymph 
nodes from AIDS victims have shown the germinal centers of the nodes disappear 
("burned out" ) in the late stages of AIDS. It has been hypothesized that this 
destruction is caused by cytolysis of HIV contaminated cells. It is theorized 
that removal and replacement of HIV impacted dendritic cells (by regular DNCB 
usage) could help to minimize the viral load of HIV in the lymphoid organs 
thus prolonging their ability to regulate immune responses.

REFERENCES
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Cameron PU, Freudenthal PS, Barker JM, Getzelter S, Inaba K, Steinman RM. 
Dendritic cells exposed to human immunodeficiency virus type-1 transmit a 
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Friedmann PS. The immunology of allergic contact dermatitis: the DNCB story. 
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Lee S, Cho CK, Kim JG, Chun SI. Therapeutic effect of dintrochlorobenzene 
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